ライフサイエンスコーパス: necrosis

1 week HFHF rat reduced ALT by 71% and reduced necrosis.

2 a to 8.3 (95% CI, 4.6 to 14.9) for avascular necrosis.

3 tules resulting in ulceration and hypodermal necrosis.

4 by inhibiting calcium flux and mPT-dependent necrosis.

5 others to care for patients with pancreatic necrosis.

6 t progression to life-threatening intestinal necrosis.

7 ors the health of cells and is stimulated by necrosis.

8 suggestive of replacement fibrosis or focal necrosis.

9 ild brush border injury without apoptosis or necrosis.

10 iated early to decrease the risk of infected necrosis.

11 optosis in cancer cells, resulting in tumour necrosis.

12 cellular ATP release, DUOX-1 production, and necrosis.

13 osis pathway in cancer cells, causing tumour necrosis.

14 ents with AKI and COVID-19 was acute tubular necrosis.

15 esenteric panniculitis, and encapsulated fat necrosis.

16 n thrombosis and pancreatic head parenchymal necrosis.

17 of a coronary artery results in swift tissue necrosis.

18 rosis is indicated in patients with infected necrosis.

19 Neutrophil depletion dampens necrosis.

20 AD patients reveal a remarkable increase of necrosis.

21 stents for endoscopic transmural drainage of necrosis.

22 8 +/- 4.3% vs. 6.43 +/- 0.29; p < 0.001) and necrosis (18.65 +/- 5.19%; p < 0.01).

23 ion in tumor growth and a 27.69% increase in necrosis 20 days post-injection compared to Dox alone IS

24 y included necrosis only (25%), teratoma +/- necrosis (20%), viable nonteratomatous germ cell tumor +

25 nastomosis, staple line or localized conduit necrosis (9%), and acute delirium (5%).

26 were treated as viable, sensitivity of tumor necrosis across readers ranged from 81% to 87%, and spec

27 d that TMNP causes synergistic apoptosis and necrosis along with cell cycle arrest at the G1-S phase

28 Both BA caused cell necrosis and apoptosis, although the former was the main

29 bility of the sarcolemma and skeletal muscle necrosis and atrophy.

30 oxal metabolism, and that protection against necrosis and cardiac IR injury bought on by ALKBH7 defic

31 ve histopathological features, such as gross necrosis and high tumor grade.

32 hed swelling in the inoculated foot and less necrosis and inflammation in the interosseous muscles.

33 required in patients with sterile pancreatic necrosis and persistent unwellness marked by abdominal p

34 xicity was evaluated by MTT assay, apoptosis/necrosis and phosphorylated-cAbl (cAbl-p).

35 elated problems that culminated in allograft necrosis and the eventual loss of the facial transplant,

36 he clinical care of patients with pancreatic necrosis and to offer concise best practice advice for t

37 sting based on their ability to induce liver necrosis and, eventually, liver cancer.

38 rminant for the extension of the spontaneous necrosis, and for the intratumoral localization of the i

39 ry responses, resulting in tissue damage and necrosis, and for this, administering an antifungal drug

40 Rates of explantation, infection, tissue necrosis, and hematoma were comparable between groups.

41 tis, characterized by neuronal degeneration, necrosis, and mononuclear leukocyte infiltrates, was obs

42 ples showed varying degrees of acute tubular necrosis, and one patient had associated widespread myog

43 o reduces the risk of wound dehiscence, skin necrosis, and seroma.

44 , cellular crescents, neutrophils, fibrinoid necrosis, and tubulointerstitial inflammation in the kid

45 sfunction was not associated with myocardial necrosis, apoptosis, inflammation, or mitochondrial perm

46 of autophagy and forms of cell death such as necrosis, apoptosis, necroptosis and pyroptosis.

47 Acute tubular necrosis, apoptosis, urinary kidney damage markers, neut

48 Smoking aggravates skin necrosis as a complication of random-pattern flap ischae

49 er CCl(4) injury despite a similar degree of necrosis as controls.

50 d posttreatment of observed anterior stromal necrosis (ASN) after long-term Intacs intracorneal ring

51 es in the breast MRI done for staging: size, necrosis, associated findings, adenopathies, and perfusi

52 nephropathy (BKVAN) 9.9%; and acute tubular necrosis (ATN with i-INT) in 5.9% of cases.

53 tic groups-SAGN, primary IgAN, acute tubular necrosis (ATN) and normal kidney (baseline transplant bi

54 e cellular rejection (ACR), or acute tubular necrosis (ATN).

55 scopic or surgical debridement with residual necrosis burden.

56 xygenase required for DNA alkylation-induced necrosis, but its function and substrates remain unclear

57 n in patients with large amounts of infected necrosis, but should be performed at referral centers wi

58 sis and promotes immunostimulatory secondary necrosis by binding to the phagocytic marker phosphatidy

59 Performance characteristics for predicting necrosis category based on LI-RADS treatment response (L

60 1R-E102Q mutant) overexpression reverses eye necrosis, climbing deficit, and firing discharge caused

61 Tumor necrosis commonly exists and predicts poor prognoses in

62 tic remnant after acute necrotizing mid-body necrosis, definitive surgical management with distal pan

63 Moreover, EPA and DHA decreased cell necrosis demonstrated by live cell imaging and transmiss

64 in a positive feedback loop, amplifying GBM necrosis development to its fullest extent.

65 V) combines with a potyvirus in maize lethal necrosis disease (MLND), a serious emerging disease worl

66 .IMPORTANCE In the past decade, maize lethal necrosis disease has caused massive crop losses in East

67 Because inhibiting platelet necrosis does not compromise hemostasis, targeting plate

68 -MARCKS), and reveal an increase of neuronal necrosis during pre-symptomatic phase and a subsequent d

69 ACTICE ADVICE 4: In patients with pancreatic necrosis, enteral feeding should be initiated early to d

70 Anti-tumor necrosis factor (anti-TNF) therapies are the most widely

71 Anti-tumor necrosis factor (anti-TNF) therapy resistance is a major

72 luding biologics (in particular, anti-tumour necrosis factor (TNF) agents).

73 ive or die in response to the cytokine tumor necrosis factor (TNF) and other inflammatory stimuli.

74 logues of SPD-304, a dual inhibitor of tumor necrosis factor (TNF) and RANKL trimerization, we identi

75 Addition of a microglial tumor necrosis factor (TNF) deficiency rescued these animals,

76 thritis have an inadequate response to tumor necrosis factor (TNF) inhibitors.

77 Excessive tumor necrosis factor (TNF) is known to cause significant path

78 ty of AVX-470, a bovine colostral anti-tumor necrosis factor (TNF) polyclonal antibody used in early

79 -induced intercellular feedback in the tumor necrosis factor (TNF) response.

80 We demonstrate that tumor necrosis factor (TNF) signaling limits M2 granuloma macr

81 le in mitophagy but did play a role in tumor necrosis factor (TNF) signaling.

82 Conversely, anti-Tumor Necrosis Factor (TNF) therapies improve depression provi

83 Since the early 2000s, anti-tumour necrosis factor (TNF) treatment has significantly improv

84 terleukin 2 (IL-2), IL-6, IL-12 (p70), tumor necrosis factor (TNF), and IL-10, was observed in mice a

85 ed CXCL8) and the expression of CXCL8, tumor necrosis factor (TNF), and other proinflammatory genes.

86 cells expressed more interferon-gamma, tumor necrosis factor (TNF), granzyme B, and perforin than CD8

87 ry, pro-inflammatory cytokines such as tumor necrosis factor (TNF), interleukin (IL)-6 and IL-8 were

88 easure serum interleukin (IL)-6, IL-8, tumor necrosis factor (TNF)-alpha and IL-1beta in hospitalized

89 levels of LRG, interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha in patients with Stage 3 per

90 7A) and 6A (UTX) play crucial roles in tumor necrosis factor (TNF)-alpha signaling in endothelial cel

91 Administration of tumor necrosis factor (TNF)-alpha, an established HIV latency

92 trigger tissue destruction and produce tumor necrosis factor (TNF)-alpha, post-effector cells acquire

93 Tumor necrosis factor (TNF)-alpha-induced protein 8 (TNFAIP8 o

94 t control the interferon response and tumour necrosis factor (TNF)-induced cytotoxicity are dominant

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

96 e exposed to interleukin (IL)1beta and tumor necrosis factor (TNF)alpha with and without UDCA.

97 e by HIV-infected MG-hBORGs, releasing tumor necrosis factor (TNF-alpha) and interleukin-1 (IL-1beta)

98 Serum levels of tumor necrosis factor -alpha and interferon-gamma were signifi

99 , glutathione, oxidative stress [OSI], tumor necrosis factor [TNF]-alpha, interleukin [IL]-1beta, mat

100 , thiopurines, methotrexate); (2) anti-tumor necrosis factor agents; (3) combination therapy; and (4)

101 The cytokine soluble tumor necrosis factor alpha (sTNFalpha) is upregulated in the

102 and also with decreased production of tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta

103 popolysaccharide-induced expression of tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-

104 s similar under control conditions but tumor necrosis factor alpha (TNF-alpha) and PKCdelta-i had a s

105 Potent agonists of NF-kappaB such as tumor necrosis factor alpha (TNF-alpha) and vgRNA failed to in

106 ion to endothelial cells inflamed with tumor necrosis factor alpha (TNF-alpha) by reducing expression

107 07a, gamma interferon (IFN-gamma), and tumor necrosis factor alpha (TNF-alpha) from ILC3; and an incr

108 ning 223Q significantly decreased both tumor necrosis factor alpha (TNF-alpha) mRNA levels and protei

109 vein ECs, we found that treatment with tumor necrosis factor alpha (TNF-alpha) or the strong oxidant

110 s were shown to promote TLR2-dependent tumor necrosis factor alpha (TNF-alpha) release from bone marr

111 otein (CRP), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) were also evaluated.

112 Here, we show that tumor necrosis factor alpha (TNF-alpha), a critical cytokine l

113 ction, including interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), and CXCL8, and identi

114 measured interleukin (IL) 1beta, IL-6, tumor necrosis factor alpha (TNF-alpha), and high-sensitivity

115 lony-stimulating factor (GCSF), MCP-1, tumor necrosis factor alpha (TNF-alpha), and IgG anti-toxin A

116 faecalis-induced DCs, while IL-1beta, tumor necrosis factor alpha (TNF-alpha), and IL-12 levels were

117 ls of gamma interferon (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha), as well as a rapid ex

118 l cytokines and chemokines, especially tumor necrosis factor alpha (TNF-alpha), CCL3, CCL4, and CCL20

119 g interleukin 6 (IL-6), IL-1alpha, and tumor necrosis factor alpha (TNF-alpha).

120 and potentiates toxicity triggered by tumor necrosis factor alpha (TNF-alpha).

121 0 (IL-10), interleukin 22 (IL-22), and tumor necrosis factor alpha (TNF-alpha).

122 tivation of proinflammatory cytokines (tumor necrosis factor alpha (TNFalpha) and interleukin 6 (IL-6

123 HP-1 human monocytic cells to generate tumor necrosis factor alpha (TNFalpha) and interleukin 8 (IL8)

124 Tumor necrosis factor alpha (TNFalpha) has emerged as a critic

125 ession of the proinflammatory cytokine tumor necrosis factor alpha (TNFalpha) in gut-associated macro

126 2) Tumor necrosis factor alpha (TNFalpha) induced HA-mediated mon

127 Tumor necrosis factor alpha (TNFalpha) is a soluble cytokine t

128 in response to interleukin-1 (IL-1) or tumor necrosis factor alpha (TNFalpha) stimulation.

129 alloprotease 17) is a key regulator of tumor necrosis factor alpha (TNFalpha), interleukin 6 receptor

130 te brain inflammation induced by local tumor necrosis factor alpha (TNFalpha), we found that uptake o

131 s issue of Blood, He et al show that a tumor necrosis factor alpha (TNFalpha)-mediated pathway regula

132 e.g., interferon gamma [IFN-gamma] and tumor necrosis factor alpha [TNF-alpha]) produced by innate ly

133 atory molecules (interleukin-6 [IL-6], tumor necrosis factor alpha [TNFalpha], matrix metalloproteina

134 e observed in ECD kidneys, except that tumor necrosis factor alpha and monocyte chemotactic protein 1

135 The metalloprotease TACE (tumor necrosis factor alpha converting enzyme) is responsible

136 f the proinflammatory cytokine soluble tumor necrosis factor alpha days after an injury sufficiently

137 s of p21, mTOR/pS6, interleukin 6, and tumor necrosis factor alpha in skin and heart tissues of aged

138 vessel density in the penumbra, higher tumor necrosis factor alpha plasma levels and lower peripheral

139 induced Toll-like receptor 4-dependent tumor necrosis factor alpha production by macrophages.

140 human monoclonal antibody specific for tumor necrosis factor alpha that has already been approved for

141 platform through the quantification of tumor necrosis factor alpha with a detection limit as low as 3

142 macrophage-colony-stimulating factor, tumor necrosis factor alpha, and interleukin (IL)-6 secretion.

143 ng monocyte chemoattractant protein 1, tumor necrosis factor alpha, and interleukin 6) through YAP as

144 n (IFN)-gamma, interleukin (IL)1-beta, tumor necrosis factor alpha, caspase-1 (CASP1), intercellular

145 This study compares levels of tumor necrosis factor alpha, IL-6, and IL-8 in critically ill

146 ), and fibronectin while up-regulating tumor necrosis factor alpha, interleukin-6, and C-X-C motif ch

147 ycation end products, interleukin-1ra, tumor necrosis factor alpha, surfactant protein D, and interle

148 ding interleukin (IL)-1beta, IL-6, and tumor necrosis factor alpha.

149 We examined the outcome of anti-tumor necrosis factor and anti-interleukin-12/interleukin-23 t

150 d protein kinase activation to control tumor necrosis factor and IL-1alpha/beta expression, and in ma

151 nd MyD88, was exquisitely sensitive to tumor necrosis factor and interleukin-17A, and persisted in ge

152 we found that host-derived cytokines tumour necrosis factor and interleukin-1alpha stimulated reacti

153 ons in key regulatory genes, including tumor necrosis factor and interleukin-1beta.

154 tibiotic treatment, neutralization of tumour necrosis factor and surgical intervention together with

155 r intolerance to immunosuppressants or tumor necrosis factor antagonists.

156 rm of the mannose receptor (CD206) and tumor necrosis factor by enzyme-linked immunosorbent assay (te

157 ) expression of glucocorticoid-induced tumor necrosis factor ligand (GITRL) was essential for inducti

158 contents; increased immunostaining for tumor necrosis factor ligand superfamily member 14; sparse mas

159 e-dependent Ripk1-independent IL-1 and tumor necrosis factor production, and were prone to cell death

160 ecroptosis, which is also dependent on tumor necrosis factor receptor (TNF-R) signaling.

161 Both orthopoxviruses encode tumor necrosis factor receptor (TNFR) homologs or viral TNFR (

162 Ligand-induced tumor necrosis factor receptor 1 (TNFR1) activation controls n

163 and +21 post-HCT: stimulation-2 (ST2), tumor necrosis factor receptor 1 (TNFR1), regenerating islet-d

164 Tumor necrosis factor receptor 1 is increased in cystic fibros

165 IL-6, IL-8, IL-10, and sTNFR1 (soluble tumor necrosis factor receptor 1) were assessed in plasma from

166 Tumor necrosis factor receptor 2 (TNFR2) is strongly upregulat

167 self-antigens, and are switched on by tumor necrosis factor receptor 2 (TNFR2).

168 ts directed at members of the CD28 or tumour necrosis factor receptor families.

169 on and that inactivation of Tregs with tumor necrosis factor receptor II (TNFR2) antagonistic antibod

170 We report here that tumor necrosis factor receptor superfamily death receptor 3 (T

171 inine ratio (uACR) and plasma soluble tumour necrosis factor receptor-1 (sTNFR1) with respect to earl

172 8, chitinase-3-like protein-1, soluble tumor necrosis factor receptor-1, procalcitonin [PCT], C-react

173 n functional and mechanistic analyses, tumor necrosis factor receptor-associated factor (TRAF)-mediat

174 ve protein, IL6, d-dimer, and systemic tumor necrosis factor receptors I and II (P <= .05).

175 n patients subsequently requiring anti-tumor necrosis factor rescue therapy.

176 tor and was promoted by cell-intrinsic tumor necrosis factor signaling.

177 Tumor necrosis factor superfamily (TNFSF) members, including T

178 a signaling molecule downstream of the tumor necrosis factor superfamily receptors such as CD27, in t

179 tolerance induction, and released more tumor necrosis factor than SPMs.

180 death, necroptosis can be triggered by tumor necrosis factor via the kinases RIPK1/RIPK3 and the effe

181 es showing IL (interleukin) 1B or TNF (tumor necrosis factor) expression as well as a foam cell-like

182 l an unexpected link between the TNF (tumour necrosis factor) inflammatory pathway, triggered by the

183 le)-1 and TF expression following TNF (tumor necrosis factor)-alpha stimulation.

184 nflammation by gene expression of TNF (tumor necrosis factor)-alpha.

185 tokines (eg, IL-17, interferon-gamma, tissue necrosis factor, granulocyte-macrophage colony-stimulati

186 or pro-inflammatory cytokines such as tumour necrosis factor, IL-1beta and IL-17.

187 growth factor beta2) and inflammation (tumor necrosis factor, interleukin 1beta).

188 Tumour necrosis factor, which suppresses the generation of acti

189 pression changes induced by short-term tumor necrosis factor-alpha (TNF) treatment were largely susta

190 with proinflammatory cytokines such as tumor necrosis factor-alpha (TNF), the master transcriptional

191 les were used to measure the levels of tumor necrosis factor-alpha (TNF-alpha) and cytokine-induced n

192 rcinoma tissues express high levels of tumor necrosis factor-alpha (TNF-alpha) and other inflammatory

193 y demonstrated that supraphysiological tumor necrosis factor-alpha (TNF-alpha) boosts glutamatergic t

194 been found to have elevated levels of Tumor Necrosis Factor-alpha (TNF-alpha) in the eye.

195 (IL-1beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) in the gingival crevic

196 r endothelial growth factor (VEGF) and tumor necrosis factor-alpha (TNF-alpha) may regulate several b

197 d carbon tetrachloride) by increasing tumour necrosis factor-alpha (TNF-alpha) production which then

198 (CI, 1.3- to 40.0-fold; P < 0.001) for tumor necrosis factor-alpha (TNF-alpha), 7.0-fold (CI, 3.5- to

199 n from GF was evaluated in response to tumor necrosis factor-alpha (TNF-alpha), IL-1beta, Escherichia

200 GSH and inflammatory mediators such as tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL

201 of the Rab3 and Rab27 small GTPases, tumour necrosis factor-alpha (TNF-alpha)-induced signalling and

202 atory interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha).

203 n of proinflammatory cytokines such as tumor necrosis factor-alpha (TNFalpha).

204 ry cytokines (including interleukin-6, tumor necrosis factor-alpha and interleukin-1beta), rebalanced

205 evels and decreased nuclear factor-kB, tumor necrosis factor-alpha and interleukin-6 gene expression

206 h decreased early gut injury and serum tumor necrosis factor-alpha compared with allogeneic controls.

207 and showed increased interleukin-8 and tumor necrosis factor-alpha concentrations.

208 characterized by interferon-gamma and tumor necrosis factor-alpha cytokine secretion by CD4(+) T cel

209 (2) -R activation also decreased serum tumor necrosis factor-alpha levels and improved cardiac dysfun

210 pression of lipopolysaccharide-induced tumor necrosis factor-alpha transcription factor 3 (LL3).

211 osed cells showed increased TNF-alpha (tumor necrosis factor-alpha) production.

212 ers (interleukin [IL]-1beta, IL-6, and tumor necrosis factor-alpha) were observed in the medium as we

213 cible nitric oxide synthase and lower tumour necrosis factor-alpha), pro-healing immune profiles (hig

214 le CD25, interleukin (IL)-6, IL-1beta, tumor necrosis factor-alpha, and IL-10 and lower levels of IL-

215 Interleukin-6 and -10, tumor necrosis factor-alpha, and insulin-like growth factor-1

216 and interleukin-1beta, interleukin-6, tumor necrosis factor-alpha, and interleukin-10 levels in vivo

217 tory factors, including interleukin-6, tumor necrosis factor-alpha, and matrix metalloproteinase-9, s

218 ad higher levels of interleukin-1beta, tumor necrosis factor-alpha, and reactive oxygen species when

219 , and -10 retained the association but tumor necrosis factor-alpha, C-reactive protein, and S-100beta

220 ion group, interleukin-6, -8, and -10, tumor necrosis factor-alpha, C-reactive protein, and S-100beta

221 Proinflammatory cytokines tumor necrosis factor-alpha, IL-1beta, IL-6, and IL-12p40 are

222 ltiple inflammatory markers, including tumor necrosis factor-alpha, interleukin-1beta, and nitric oxi

223 nflammatory gene expression (IL-1beta, tumor necrosis factor-alpha, intracellular adhesion molecule 1

224 otegerin]), 3 inflammatory biomarkers (tumor necrosis factor-alpha, sTNFRI [soluble tumor necrosis fa

225 ntibody, the target cytokine, that is, tumor necrosis factor-alpha, was measured in terms of rotation

226 s: inducible nitric-oxide synthase and tumor necrosis factor-alpha, when cultured under hyperglycemic

227 cell-mediated and interferon-gamma and tumor necrosis factor-alpha-induced cell death compared to Tre

228 efore and after ILP with melphalan and tumor necrosis factor-alpha.

229 terleukin-12p40, interferon-gamma and tumour necrosis factor-alpha.

230 Tumor necrosis factor-like cytokine 1A (TL1A, TNFSF15) is impl

231 necrosis factor-alpha, sTNFRI [soluble tumor necrosis factor-receptor I], and interleukin-6), YKL-40

232 The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL

233 conatumumab, an antibody that targets tumor necrosis factor-related apoptosis-inducing ligand recept

234 resymptomatic activation of IL-17- and tumor necrosis factor-related pathways.

235 es (IL [interleukin] 1B, IL6, and TNF [tumor necrosis factor]).

236 vein levels of pro-inflammatory marker tumor necrosis-factor (TNF)-alpha.

237 ecrosis) and surgery (wound infections, flap necrosis, fistulas,...).

238 Degree of tumor necrosis found on explant has been associated with recur

239 cyte autophagy promotes IL-1beta/TNF-induced necrosis from impaired energy homeostasis and lysosomal

240 Patients who achieved extensive or complete necrosis had better RFS, supporting the practice of neoa

241 Substantial necrosis helped identify 65% (17 of 26; 95% CI: 44%, 83%

242 c regression analysis identified substantial necrosis, high serum alpha-fetoprotein (AFP) level (>100

243 reased tumor vasculature and increased tumor necrosis in comparison with tumors treated with monother

244 related to anthocyanin production and early necrosis in genome-wide association analyses.

245 Underscoring the role of platelet necrosis in PNA formation, we observed a significant num

246 The lead compound 48c, induced necrosis in several mutant and FLT3-resistant AML cell l

247 severe COVID-19 in China found acute tubular necrosis in the kidney, a few patient reports have also

248 acid residues are individually mutated, the necrosis-inducing activity is completely abolished.

249 these by mutagenesis and in planta assays of necrosis induction by expression in N. benthamiana, as w

250 with significantly attenuated renal tubular necrosis, inflammation, and apoptosis when compared to P

251 Significant ablation-related esophageal necrosis, inflammation, and fibrosis were seen in all ra

252 ted normal portal tract, with no parenchymal necrosis, inflammation, fibrosis, or other pathologic ch

253 As expected, necrosis is Hla dependent in the presence or absence of

254 5: Drainage and/or debridement of pancreatic necrosis is indicated in patients with infected necrosis

255 ed by mitochondria-associated apoptosis, and necrosis is likely to contribute to the toxicities.

256 antibiotics to prevent infection of sterile necrosis is not recommended.

257 BEST PRACTICE ADVICE 3: When infected necrosis is suspected, broad-spectrum intravenous antibi

258 At multivariable analysis, substantial necrosis (odds ratio = 32; 95% confidence interval [CI]

259 Avascular necrosis of femoral head (AVNFH) is a debilitating disea

260 liver fibrosis (chronic damage), as well as necrosis of hepatocytes in zone 3 of the Rappaport acinu

261 , initiates cell death, leading to extensive necrosis of leaf tissues.

262 ade, apoptosis, genotoxicity, and ultimately necrosis of neuronal cells.

263 enterocolitis (NEC) is an inflammatory bowel necrosis of premature infants and an orphan disease with

264 muscle cells, ultimately resulting in rapid necrosis of the entire nervous system and muscle cells t

265 nd hla DeltafakA mutants are unable to cause necrosis of the skin.

266 ed rejection (CAMR), leading to irreversible necrosis of the tissue.

267 Apoptosis, but not necrosis, of donor cells was found associated with robus

268 howed complete, extensive, and partial tumor necrosis on histopathology.

269 P < 0.001) were associated with shorter PFS; necrosis on pathology (HR, 0.42, P = 0.043) was associat

270 Pathology included necrosis only (25%), teratoma +/- necrosis (20%), viable

271 ell detachment process induced by apoptosis, necrosis or cell lysis substances, respectively.

272 Fat necrosis or inflammation are common findings in abdomina

273 re was more likely in patients with infected necrosis or NP disease duration >=6 months.

274 d for culture-proven infection in pancreatic necrosis or when infection is strongly suspected (ie, ga

275 lications derived from radiotherapy (mucosal necrosis, osteoradionecrosis, vasculopathy, cerebral rad

276 arding anastomotic leak (P = 0.596), conduit necrosis (P = 0.524), chyle leak (P = 0.427), pneumonia

277 endritic cells (DC) respond to cardiomyocyte necrosis, present cardiac antigen to T cells, and potent

278 mediator of necrosis, we found that platelet necrosis regulates tissue damage and outcomes during isc

279 preclinical/prodromal YAP-dependent neuronal necrosis represents a target for AD therapeutics.

280 presents cause or consequence of local tumor necrosis requires further study.

281 udies demonstrated that IL-1beta/TNF-induced necrosis resulted from lysosomal permeabilization and re

282 dence indicated that iNPWT also reduced skin necrosis (RR 0.49, 95% CI: 0.33-0.74), seroma (RR 0.43,

283 NPWT may also prevent wound dehiscence, skin necrosis, seroma, and hematoma.

284 biotics with ability to penetrate pancreatic necrosis should be favored (eg, carbapenems, quinolones,

285 ere characterized by areas of subendocardial necrosis surrounded by a rim of fibrosis.

286 Histological examination demonstrated tissue necrosis surrounded by acute and chronic inflammation an

287 ncide with flowering result in leaf wilting, necrosis, tassel browning, and sterility, a stress condi

288 n GBM mouse model, neutrophils coincide with necrosis temporally and spatially.

289 AT-RasGAP(317-326) kills cells via a form of necrosis that relies on the physical disruption of the p

290 In three patients with glandular necrosis, the density of iodine was 1.53mg/ml.

291 n, lobular cholestasis, and acute liver cell necrosis, together with central vein thrombosis.

292 , lactate dehydrogenase (LDH) activity, cell necrosis, transepithelial electrical resistance (TEER),

293 sfunction, premature zymogen activation, and necrosis, ultimately leading to pancreatitis.

294 rimary tumors revealed enhanced intratumoral necrosis upon silencing of tumor cell Angpt2 expression

295 (BE(2)-C cells showed signs of apoptosis and necrosis upon treatment with Tat-A and Tat-B.

296 1 and caspase-8 and inhibition of programmed necrosis via TLR4 and TNFR1.

297 etion of cyclophilin D (CypD), a mediator of necrosis, we found that platelet necrosis regulates tiss

298 lymphocytes (TIL), PD1 expression, and tumor necrosis while slowing tumor growth and modestly increas

299 be reserved for those patients with limited necrosis who do not adequately respond to endoscopic tra

300 managing patients with walled-off pancreatic necrosis (WON).