ライフサイエンスコーパス: necrotize

1 There is evidence that MPO-ANCA cause necrotizing and crescentic glomerulonephritis (NCGN) and

2 Necrotizing and crescentic GN (NCGN) with a paucity of g

3 s discussed in thrombotic microangiopathies, necrotizing and crescentic GN, acute tubular necrosis, a

4 Necrotizing anterior scleritis was more commonly seen in

5 ght patients with active, noninfectious, non-necrotizing anterior scleritis with a scleral inflammato

6 ve participants with active, autoimmune, non-necrotizing anterior scleritis with scleral inflammatory

7 icacy of gevokizumab in the treatment of non-necrotizing anterior scleritis.

8 Necrotizing autoimmune myopathy (NAM) is characterized p

9 including rhabdomyolysis and statin-induced necrotizing autoimmune myopathy (SINAM), are rare.

10 Necrotizing autoimmune myopathy was idiopathic in half o

11 We systematically studied the incidence of necrotizing changes in adult patients with pneumococcal

12 Necrotizing changes in the lungs were seen in 6.6% of a

13 Goats developed various effects, including necrotizing colitis, pulmonary edema, and hydropericardi

14 is central to ANCA-associated vasculitis and necrotizing crescentic glomerulonephritis (NCGN).

15 gan, including the kidneys, where they cause necrotizing crescentic glomerulonephritis.

16 pothesis that endothelial NF-kappaB mediates necrotizing crescentic GN (NCGN) and provides a specific

17 ophil cytoplasmic antibody (ANCA)-associated necrotizing crescentic GN (NCGN) is incompletely underst

18 CA-activated phagocytes cause vasculitis and necrotizing crescentic GN (NCGN).

19 sgenic mice, evidenced by the development of necrotizing crescentic GN, albuminuria, renal impairment

20 With the emergence of necrotizing/crescentic glomerulonephritis, approximately

21 tional immunizations were needed to induce a necrotizing/crescentic glomerulonephritis.

22 xperimental autoimmune glomerulonephritis or necrotizing/crescentic glomerulonephritis.

23 eukocidin (PVL) is most likely causative for necrotizing diseases, but the precise pathogenic mechani

24 Leigh syndrome (LS) is a subacute necrotizing encephalomyelopathy with gliosis in several

25 liver function and Leigh syndrome (subacute necrotizing encephalomyelopathy) seen in association wit

26 ific acute encephalopathy syndromes (4 acute necrotizing encephalopathy, 1 acute infantile encephalop

27 is required for CN3685 to cause haemorrhagic necrotizing enteritis, apparently because the Agr-like s

28 3 to 1.00; P=0.045) and an increased rate of necrotizing enterocolitis (10.4% vs. 8.0%; relative risk

29 (17.5% [95% CI, 16.5%-18.6%]), and death or necrotizing enterocolitis (19.3% [95% CI, 18.1%-20.4%]).

30 there were increases in deaths attributed to necrotizing enterocolitis (30 [95% CI, 27 to 34] vs. 23

31 urvivors (23.3%, 19.1%, and 11.7%), death or necrotizing enterocolitis (48.1%, 37.1%, and 32.5%), and

32 in mortality (AOR, 0.98; 95% CI, 0.70-1.37), necrotizing enterocolitis (AOR, 0.88; 95% CI, 0.65-1.20)

33 Mental development was most impaired by necrotizing enterocolitis (d = -0.40; P < .001) and meni

34 Motor development was most impaired by necrotizing enterocolitis (d = -0.66; P < .001).

35 Necrotizing enterocolitis (NEC) affects up to 10% of pre

36 LNT were shown to protect neonatal rats from necrotizing enterocolitis (NEC) and are good therapeutic

37 d blood cell (RBC) transfusion and anemia to necrotizing enterocolitis (NEC) are conflicting.

38 Necrotizing enterocolitis (NEC) continues to be a major

39 Necrotizing enterocolitis (NEC) develops in response to

40 Necrotizing enterocolitis (NEC) has long remained a sign

41 ant manifestation of severe diseases such as necrotizing enterocolitis (NEC) in neonates or bowel wal

42 Necrotizing enterocolitis (NEC) is a devastating disease

43 Necrotizing enterocolitis (NEC) is a devastating inflamm

44 Necrotizing enterocolitis (NEC) is a devastating intesti

45 Necrotizing enterocolitis (NEC) is a major cause of morb

46 Necrotizing enterocolitis (NEC) is a major cause of neon

47 Necrotizing enterocolitis (NEC) is a severe disease of t

48 Necrotizing enterocolitis (NEC) is a severe disease that

49 Necrotizing enterocolitis (NEC) is an inflammatory disea

50 Necrotizing enterocolitis (NEC) is one of the most serio

51 Necrotizing enterocolitis (NEC) is the leading cause of

52 Necrotizing enterocolitis (NEC) is the most common and s

53 Necrotizing enterocolitis (NEC) is the most common gastr

54 rentiation and is involved in development of necrotizing enterocolitis (NEC) of the immature intestin

55 The pathophysiology of necrotizing enterocolitis (NEC) remains poorly understoo

56 r is the consequence of intestinal injury in necrotizing enterocolitis (NEC) remains unknown.

57 the proinflammatory cascade, is activated in necrotizing enterocolitis (NEC), a devastating condition

58 t of lung disease in the setting of neonatal necrotizing enterocolitis (NEC), a life-threatening gast

59 ure and role of the intestinal leukocytes in necrotizing enterocolitis (NEC), a severe disease affect

60 y result in antibiotic resistance, fungemia, necrotizing enterocolitis (NEC), and mortality.

61 y infections, otitis media, gastroenteritis, necrotizing enterocolitis (NEC), and sudden infant death

62 the widespread use of plain films to detect necrotizing enterocolitis (NEC), it is considered a time

63 reast milk (HBM) attenuates the incidence of necrotizing enterocolitis (NEC), which remains a leading

64 ession, which can lead to the development of necrotizing enterocolitis (NEC)--a devastating inflammat

65 possible pregnancy-related risk factors for necrotizing enterocolitis (NEC)-associated deaths during

66 diseases characterized by ISC loss including necrotizing enterocolitis (NEC).

67 is supposedly associated with development of necrotizing enterocolitis (NEC).

68 riate analysis, SL mortality predictors were necrotizing enterocolitis (NEC; surgical odds ratio, 5.9

69 pathy of prematurity (stage 3 or higher), or necrotizing enterocolitis (stages 2-3).

70 ve been implicated as a pathogenic factor in necrotizing enterocolitis and inflammatory bowel disease

71 premature newborns has been shown to prevent necrotizing enterocolitis and reduce all-cause mortality

72 Infants with necrotizing enterocolitis born into midlevel hospitals (

73 ptation to small-bowel resection (SBR) after necrotizing enterocolitis expands absorptive surface are

74 given enterally may reduce the incidence of necrotizing enterocolitis in preterm infants.

75 diabetes, nonalcoholic fatty liver disease, necrotizing enterocolitis in very low birth weight infan

76 levance was suggested, as TLR4 activation in necrotizing enterocolitis led to reduced proliferation a

77 Late-onset invasive infection or necrotizing enterocolitis occurred in 32% of infants (19

78 Necrotizing enterocolitis occurred less frequently in th

79 Necrotizing enterocolitis occurred more frequently in in

80 CI, 0.58-0.78) and the combined outcomes of necrotizing enterocolitis or death and severe intraventr

81 dio-pulmonary bypass, as well as in neonatal necrotizing enterocolitis or persistent ductus arteriosu

82 r retinopathy of prematurity and surgery for necrotizing enterocolitis or spontaneous intestinal perf

83 Interestingly, we find that necrotizing enterocolitis patients also exhibit decrease

84 Infants with necrotizing enterocolitis represent a high-risk subgroup

85 ere intraventricular hemorrhage and death or necrotizing enterocolitis was lowest among infants born

86 The occurrence of necrotizing enterocolitis was significantly higher in th

87 of the study, just 28.6% of the infants with necrotizing enterocolitis were born into high-level, hig

88 nary dysplasia, severe cerebral lesions, and necrotizing enterocolitis).

89 2, periventricular leukomalacia >grade 1, or necrotizing enterocolitis).

90 sed sample of 30 566 VLBW infants, 1879 with necrotizing enterocolitis, according to the level of car

91 dities before PDA closure, including sepsis, necrotizing enterocolitis, and a dependence on mechanica

92 aturity, severe intraventricular hemorrhage, necrotizing enterocolitis, and chronic lung disease amon

93 s, hearing loss, bronchopulmonary dysplasia, necrotizing enterocolitis, and severe retinopathy of pre

94 om BEC on premature infants with and without necrotizing enterocolitis, and successfully provided a t

95 iventricular or intraventricular hemorrhage, necrotizing enterocolitis, aspiration, retinopathy of pr

96 he following morbidities: late-onset sepsis, necrotizing enterocolitis, bronchopulmonary dysplasia, p

97 Necrotizing enterocolitis, defined as Bell stage 2 or gr

98 who survived more than 12 hours, were severe necrotizing enterocolitis, infection, bronchopulmonary d

99 Infections and necrotizing enterocolitis, major causes of mortality and

100 hemorrhage, bronchopulmonary dysplasia, and necrotizing enterocolitis, most therapeutic approaches h

101 nography, severe retinopathy of prematurity, necrotizing enterocolitis, or late-onset sepsis) by 36 w

102 of serious infection (sepsis or meningitis), necrotizing enterocolitis, or mortality during the first

103 ystic periventricular leukomalacia, surgical necrotizing enterocolitis, or stage 3 or greater retinop

104 ites of death or bronchopulmonary dysplasia, necrotizing enterocolitis, retinopathy of prematurity, a

105 It also decreases the prevalence of necrotizing enterocolitis, sepsis, and intraventricular

106 PN significantly affects risk of mortality, necrotizing enterocolitis, sepsis, chronic lung disease,

107 onary hemorrhage but not with differences in necrotizing enterocolitis, severe bronchopulmonary dyspl

108 No differences in rates of necrotizing enterocolitis, severe bronchopulmonary dyspl

109 etinopathy of prematurity requiring surgery, necrotizing enterocolitis, spontaneous intestinal perfor

110 The frequencies of air leaks and necrotizing enterocolitis, the duration of respiratory s

111 Chorioamnionitis, necrotizing enterocolitis, white matter injury on crania

112 ntral nervous system injury decreased, while necrotizing enterocolitis-related deaths increased.

113 rain was common to all infants who developed necrotizing enterocolitis.

114 on, a process that may lead to diseases like necrotizing enterocolitis.

115 am, urinary tract, or cerebrospinal fluid or necrotizing enterocolitis.

116 ch were profoundly depleted in newborns with necrotizing enterocolitis.

117 ther this practice reduces the prevalence of necrotizing enterocolitis.

118 so a trend towards a diminished incidence of necrotizing enterocolitis.

119 en microbes and host immune elements such as necrotizing enterocolitis.

120 n of ISCs contributes to the pathogenesis of necrotizing enterocolitis.

121 ncovered, such as the transfusion-associated necrotizing enterocolitis.

122 d incidence of neonatal bacterial sepsis and necrotizing enterocolitis.

123 s such as intestinal atresias, volvulus, and necrotizing enterocolitis.

124 h postnatal intestinal pathologies including necrotizing enterocolitis.

125 achieve the rate from the best quartile for necrotizing enterocolitis.

126 re intraventricular hemorrhage, and death or necrotizing enterocolitis.

127 ities in infants who did and did not develop necrotizing enterocolitis.

128 -specific antigen level developed postbiopsy necrotizing epididymo-orchitis (requiring orchiectomy) a

129 Cytotoxic necrotizing factor 1 (CNF1) and hemolysin (Hly) are toxi

130 Cytotoxic necrotizing factor 1 (CNF1) and hemolysin (HlyA1) are to

131 secrete the Rho protein activator cytotoxic necrotizing factor-Y (CNF-Y), but it has been unclear ho

132 ore chronic comorbidities than patients with necrotizing fasciitis (20 [87.0%] vs 17 [54.8%]; P = .02

133 or patients with cellulitis vs patients with necrotizing fasciitis (3 [2-5] vs 5 [3-11]; P = .01), wh

134 slightly younger and had a higher degree of necrotizing fasciitis (56% vs 14%).

135 known as strep throat) to severely invasive necrotizing fasciitis (also known as the flesh-eating sy

136 n = 23; mean [SD] age, 57.2 [17.7] years) or necrotizing fasciitis (n = 31; mean [SD] age, 54.3 [13.5

137 Necrotizing fasciitis (NF) caused by flesh-eating bacter

138 Shock frequently complicates necrotizing fasciitis (NF) caused by group A Streptococc

139 erile site or from a wound in a patient with necrotizing fasciitis (NF) or streptococcal toxic shock

140 hould maintain a high clinical suspicion for necrotizing fasciitis and distinguish it from more commo

141 than the carriage strain in a mouse model of necrotizing fasciitis and had enhanced growth ex vivo in

142 mic invasive infections worldwide, including necrotizing fasciitis and toxic shock syndrome.

143 p throat") to invasive conditions, including necrotizing fasciitis and toxic shock syndrome.

144 itis and skin infections to life-threatening necrotizing fasciitis and toxic shock syndrome.

145 sociated with invasive infections, including necrotizing fasciitis and toxic shock syndrome.

146 itis and impetigo to severe outcomes such as necrotizing fasciitis and toxic shock syndrome.

147 treptococcal toxic shock syndrome (STSS) and necrotizing fasciitis are the 2 most severe invasive man

148 the reason for ICU admission in 23 patients, necrotizing fasciitis in 31 patients, and other diagnose

149 this report, we present a case of multifocal necrotizing fasciitis in a healthy adult patient, second

150 Current therapeutic regimens for necrotizing fasciitis include surgical debridement and t

151 Periocular necrotizing fasciitis is a rare but potentially devastat

152 terature pertinent to S. marcescens-mediated necrotizing fasciitis is also reviewed.

153 Necrotizing fasciitis is often confused for cellulitis a

154 As seen in these 5 cases, periocular necrotizing fasciitis may cause severe visual loss more

155 We report the first case of necrotizing fasciitis of the chest wall due to infection

156 k thus aimed to address whether CLI improves necrotizing fasciitis outcome by modulating virulence fa

157 We report 5 cases of periocular necrotizing fasciitis resulting in severe vision loss, 3

158 a pathogen that causes both invasive (e.g., necrotizing fasciitis) and noninvasive (e.g., pharyngiti

159 GAS), the causative agent of pharyngitis and necrotizing fasciitis, secretes the potent cysteine prot

160 fection (streptococcal toxic shock syndrome, necrotizing fasciitis, septic shock, or GAS cellulitis w

161 h cellulitis and patients with patients with necrotizing fasciitis, Staphylococcus aureus (10 [43.5%]

162 itically ill on admission than patients with necrotizing fasciitis, they have more chronic comorbidit

163 istered as soon as possible to patients with necrotizing fasciitis, while our in vitro studies emphas

164 e-threatening invasive infections, including necrotizing fasciitis.

165 irulence in animal models of pharyngitis and necrotizing fasciitis.

166 red from nonhuman primates with experimental necrotizing fasciitis.

167 litis and to compare them with patients with necrotizing fasciitis.

168 od and reduced virulence in a mouse model of necrotizing fasciitis.

169 d we review literature on this rare cause of necrotizing fasciitis.

170 tions to life-threatening infections such as necrotizing fasciitis.

171 the virulence phenotype in a mouse model of necrotizing fasciitis.

172 n nonhuman primate models of pharyngitis and necrotizing fasciitis.

173 life-threatening invasive infections such as necrotizing fasciitis.

174 d to be less severely ill than patients with necrotizing fasciitis.

175 Streptococcus anginosus constellatus causing necrotizing fasciitis.

176 P53 is a primary isolate from a patient with necrotizing fasciitis.

177 nificantly less virulent in a mouse model of necrotizing fasciitis.

178 tia marcescens is an extremely rare cause of necrotizing fasciitis.

179 sed virulence in a nonhuman primate model of necrotizing fasciitis.

180 and increased virulence in a mouse model of necrotizing fasciitis.

181 uding streptococcal toxic shock syndrome and necrotizing fasciitis.

182 cause illnesses ranging from pharyngitis to necrotizing fasciitis.

183 rom a nonhuman primate experimental model of necrotizing fasciitis.

184 infections such as toxic shock syndrome and necrotizing fasciitis.

185 type virulence phenotype in a mouse model of necrotizing fasciitis.

186 inflammation in the central nervous system; necrotizing focal myelitis in the cervical spinal cord;

187 en in the pituitary can cause an aggressive (necrotizing) form of hypophysitis through type IV (T-cel

188 Focal and segmental necrotizing glomerular lesions with crescents, mimicking

189 vasculitis that often manifests as focal and necrotizing glomerulonephritis and renal failure.

190 T-cell clone to Rag1(-/-) mice induced focal necrotizing glomerulonephritis when glomerular MPO depos

191 V)NC1] develop anti-GBM antibodies and focal necrotizing glomerulonephritis with crescent formation.

192 Pauci-immune focal necrotizing GN (piFNGN) is usually associated with ANCAs

193 Using an established murine model of focal necrotizing GN mediated by autoimmunity to MPO (autoimmu

194 xic effect of NET-related histone release in necrotizing GN.

195 es to myeloperoxidase, and more severe focal necrotizing GN.

196 tion on chest imaging, and poorly formed non-necrotizing granulomas on pathology.

197 al mortality in conjunction with a fulminant necrotizing hepatitis.

198 inical course is marked by rapidly worsening necrotizing infection, leading to very poor outcomes des

199 These findings explain why necrotizing infections mainly develop in serum-free spac

200 istopathological examination revealed severe necrotizing inflammation in various organs, most promine

201 nephritis, and/or severe systemic multiorgan necrotizing inflammation.

202 cases of chronic pancreatitis, a progressive necrotizing inflammatory disease that can result in panc

203 Over time, the neutrophil-rich acute necrotizing lesions cause the accumulation of more lymph

204 Hypoxic necrotizing lesions rendered moxifloxacin less active.

205 arterial smooth muscle cells and deposits in necrotizing lesions.

206 microbial defence uniformly develop hypoxic necrotizing lung lesions, widely observed in human TB.

207 It has a lethal canine equivalent: necrotizing meningoencephalitis.

208 ith autoimmune myopathy have a predominantly necrotizing muscle biopsy with minimal lymphocytic infil

209 s the spectrum of diseases associated with a necrotizing muscle biopsy.

210 Immune-mediated necrotizing myopathies (IMNM) may be associated with eit

211 antibodies found in patients with autoimmune necrotizing myopathies recognize signal recognition part

212 ated with dermatomyositis and the autoimmune necrotizing myopathies.

213 ents with dermatomyositis and the autoimmune necrotizing myopathies.

214 Immune-mediated necrotizing myopathy (IMNM) is considered one of the idi

215 ients with statin-associated immune-mediated necrotizing myopathy and, less commonly, in statin-unexp

216 In a subgroup, an autoimmune necrotizing myopathy develops that persists after discon

217 One patient with severe necrotizing myopathy died.

218 t evidence now suggests that immune-mediated necrotizing myopathy is not one disease, but can be divi

219 A decade ago, immune-mediated necrotizing myopathy was recognized as a distinct form o

220 ients with dermatomyositis, polymyositis, or necrotizing myopathy, and 0/20 (0%) age-matched healthy

221 ntly identified statin-associated autoimmune-necrotizing myopathy.

222 d SLO toxins to virulence in mouse models of necrotizing myositis, bacteremia, and skin and soft tiss

223 ins are equally impaired in ability to cause necrotizing myositis.

224 ernatively, statins can induce an autoimmune necrotizing myositis.

225 sues became progressively more fibrinous and necrotizing over time.

226 At least 30% of patients with infected necrotizing pancreatitis are successfully treated with c

227 Between 1997 and 2013, patients with necrotizing pancreatitis at the Liverpool Pancreas Cente

228 n vivo in the course of taurocholate-induced necrotizing pancreatitis in rats and in vitro in rat pan

229 aurocholate into the pancreatic duct induced necrotizing pancreatitis in the head of pancreas and lig

230 Most patients with infected necrotizing pancreatitis require necrosectomy.

231 Acute necrotizing pancreatitis was induced by i.p. administrat

232 gastrointestinal tract perforation, 21 acute necrotizing pancreatitis).

233 into interstitial edematous pancreatitis and necrotizing pancreatitis, (c) distinguish an early phase

234 In patients with infected necrotizing pancreatitis, endoscopic necrosectomy reduce

235 lure; this makes the pancreas susceptible to necrotizing pancreatitis.

236 ea of intra-parenchymal necrosis, indicating necrotizing pancreatitis.

237 g catheter drainage for (suspected) infected necrotizing pancreatitis.

238 for success of catheter drainage in infected necrotizing pancreatitis.

239 2), multifocal lymphadenopathy (n = 2), and necrotizing pneumonia (n = 1).

240 of codY increased the virulence of USA300 in necrotizing pneumonia and skin infection.

241 s aureus (CA-MRSA) causes severe hemorrhagic necrotizing pneumonia associated with high mortality.

242 lveolar capillary destruction in hemorrhagic/necrotizing pneumonia caused by CA-MRSA and offer novel

243 Staphylococcus aureus necrotizing pneumonia is a life-threatening disease that

244 ive sudden, massive loss of lung tissue from necrotizing pneumonia or acute respiratory distress synd

245 A rabbit model of necrotizing pneumonia using MRSA clone USA300 was used t

246 with severe skin and soft tissue infections, necrotizing pneumonia, and eye infections.

247 th cystic fibrosis (CF) and can cause severe necrotizing pneumonia, which is often fatal.

248 USA300 is the predominant strain that causes necrotizing pneumonia.

249 ng inflammation and, in some cases, a lethal necrotizing pneumonia.

250 survival outcomes in a rabbit model of MRSA necrotizing pneumonia.

251 nfluenza virus and PVL act together to cause necrotizing pneumonia: an influenza infection activates

252 rgic bronchopulmonary aspergillosis, chronic necrotizing pulmonary aspergillosis, or invasive aspergi

253 -37 with extracellular actin was observed in necrotized regions of samples from oral lesions.

254 ime of conversion and progressed to a severe necrotizing rejection early despite an unaltered baselin

255 inal detachment repair, endophthalmitis, and necrotizing retinitis were excluded, as were those with

256 a, brownish exudates in anterior chamber and necrotizing retinitis within hours despite immediate ini

257 irst IgM test had a greater risk of incident necrotizing retinochoroiditis (hazard ratio = 4.47, 95%

258 The increased risk of late necrotizing retinochoroiditis associated with isolated f

259 al manifestation of T gondii infection, with necrotizing retinochoroiditis occurring months or years

260 The incidence of recurrent necrotizing retinochoroiditis was 10.5/100 PY.

261 ar involvement at baseline, the incidence of necrotizing retinochoroiditis was 6.4/100 PY.

262 Incident necrotizing retinochoroiditis was more common among thos

263 ut clinically apparent retinal necrosis] and necrotizing retinochoroiditis) at initial examination (b

264 inal whitening), without clinically apparent necrotizing retinochoroiditis.

265 ith focal retinal whitening only and 13 with necrotizing retinochoroiditis.

266 We present a case of hepatosplenic necrotizing sarcoid granulomatosis, a variant form of "c

267 In general, patients with necrotizing scleritis (n = 15) had a poorer outcome.

268 n vision in patients with scleritis included necrotizing scleritis (odds ratio [OR], 6.63; P<0.001),

269 otentially lethal (OR = 17.41, P=0.007), and necrotizing scleritis (OR = 4.73, P = 0.026).

270 (80.0%) occurred most often in patients with necrotizing scleritis (P<0.0001 for each).

271 Patients with necrotizing scleritis may respond to IMT, mainly alkylat

272 esent as highly invasive infections, such as necrotizing skin and soft tissue infections (NSSTI).

273 erans is known to cause Buruli ulcer (BU), a necrotizing skin disease leading to extensive cutaneous

274 Buruli ulcer (BU) is a necrotizing skin disease most prevalent among West Afric

275 virulence contribution in a murine model of necrotizing skin infection is largely driven by its abil

276 lence factor that enables CA-MRSA to produce necrotizing skin infections by allowing the bacteria to

277 isystem autoimmune diseases characterized by necrotizing small- to medium-vessel vasculitis and the p

278 ococcus (GAS) patients, including sepsis and necrotizing soft tissue infections (NSTIs).

279 research on immunocompromised patients with necrotizing soft-tissue infection (NSTI).

280 Necrotizing soft-tissue infection-associated in-hospital

281 n as a potential therapeutic in SAg-mediated necrotizing soft-tissue infection.

282 GAS bacterial infection in a murine model of necrotizing soft-tissue infection.

283 Necrotizing soft-tissue infections (NSTI) have high morb

284 Increased awareness of fungi as a cause of necrotizing soft-tissue infections after a natural disas

285 to more severe forms of infection, including necrotizing stromal keratitis and herpes simplex encepha

286 d to control T. gondii infection and died of necrotizing TE before day 77.

287 ity and utility of this approach by rescuing necrotizing tissues and whole limbs using two murine mod

288 n the CNS as well as clear histopathology of necrotizing vasculitis and hemorrhage in the brain.

289 Histopathologic analysis of the skin showed necrotizing vasculitis in biopsy samples from 40 of 50 c

290 dy-associated (ANCA-associated) small vessel necrotizing vasculitis is caused by immune-mediated infl

291 ic infectious trigger of paralyzing systemic necrotizing vasculitis most severely affecting skeletal

292 Polyarteritis nodosa is a form of necrotizing vasculitis of small and medium-sized arterie

293 et vessel wall, which may participate in the necrotizing vasculitis of the kidney during this disease

294 atosis with polyangiitis (GPA) is a systemic necrotizing vasculitis that is associated with granuloma

295 Polyarteritis nodosa is a systemic necrotizing vasculitis with a pathogenesis that is poorl

296 Histology of EGPA shows tissue eosinophilia, necrotizing vasculitis, and eosinophil-rich granulomatou

297 localized in typical PDNS lesions, including necrotizing vasculitis, glomerulonephritis, granulomatou

298 ctures and evidence of glandular atrophy and necrotizing vasculitis.

299 interact with the endothelium, resulting in necrotizing vasculitis.

300 vels associated with development of systemic necrotizing vasculitis.