ライフサイエンスコーパス: invasive disease

1 ficant fraction of patients will progress to invasive disease.

2 of hypervirulent GAS may lead to clusters of invasive disease.

3 cal nasopharyngeal carriage to pneumonia and invasive disease.

4 At least 43% of 476 specimens contained invasive disease.

5 rrelated with susceptibility to neonatal GBS invasive disease.

6 ococcus (GBS) is a leading cause of neonatal invasive disease.

7 n and soft tissue infection, and 2 cases had invasive disease.

8 f DCIS is worthwhile in prevention of future invasive disease.

9 ly discovered to have the potential to cause invasive disease.

10 differences in the incidence of early-onset invasive disease.

11 d disease severity and persistence following invasive disease.

12 tase Ptpn1 (encoding PTP1B) enables a highly invasive disease.

13 e transmitted to the newborn, causing severe invasive disease.

14 d calponin expression on DCIS progression to invasive disease.

15 differentiation occurs before transition to invasive disease.

16 The primary end point was survival free from invasive disease.

17 nt sugar encountered by S. pneumoniae during invasive disease.

18 h generally lacked the genes associated with invasive disease.

19 DCIS, a necessary step before development of invasive disease.

20 oad-spectrum efficacy against staphylococcal invasive disease.

21 ents that promote the progression of DCIS to invasive disease.

22 ithelial neoplasia after exclusion of occult invasive disease.

23 itate the progression of breast cancer to an invasive disease.

24 en isoform of Col III becomes upregulated in invasive disease.

25 , with 21% and 27%, respectively, developing invasive disease.

26 from acute otitis media to life-threatening invasive disease.

27 serotype 1 has a high likelihood of causing invasive disease.

28 evels of capsule to promote colonization and invasive disease.

29 re the most common serotypes associated with invasive disease.

30 olonization but a higher propensity to cause invasive disease.

31 ce, it is not associated with progression to invasive disease.

32 found in blood specimens from patients with invasive disease.

33 ht mechanisms whose perturbation may lead to invasive disease.

34 were enrolled in the study, of which 90% had invasive disease.

35 of genes typically involved in localized and invasive disease.

36 patients (14%) were downstaged to non-muscle invasive disease.

37 with both host and pathogen determinants of invasive disease.

38 high rates of pneumococcal colonization and invasive disease.

39 sue infections and are comparatively rare in invasive disease.

40 nous dissemination in compromised hosts with invasive disease.

41 ow this important human pathogen establishes invasive disease.

42 d site (n=28); 18 (64%) were associated with invasive disease.

43 red to risk of recurrence and progression to invasive disease.

44 ci disseminate from the nasopharynx to cause invasive disease.

45 recurrent skin and soft tissue infection, or invasive disease.

46 irming the enzyme's role as a contributor to invasive disease.

47 tients either present with or develop muscle-invasive disease.

48 both commensalism and dissemination to cause invasive disease.

49 t occurs during the progression of cancer to invasive disease.

50 gram is relevant to malignant progression in invasive disease.

51 phagocytic clearance more effectively during invasive disease.

52 increased neutrophils in the airway and more invasive disease.

53 No unique patterns were associated with invasive disease.

54 aryngeal colonization but did not affect GAS invasive disease.

55 s carried as a commensal not associated with invasive disease.

56 oportions of various Candida species causing invasive disease.

57 promote fungal translocation and facilitate invasive disease.

58 g by neutrophils and more capable of causing invasive disease.

59 occal factors are involved in progression to invasive disease.

60 ated DICER1 is significantly associated with invasive disease.

61 al population biology and a prerequisite for invasive disease.

62 K1 inhibitors as therapeutics for preventing invasive disease.

63 east cancer present with more aggressive and invasive disease.

64 mophilus influenzae are major causes of this invasive disease.

65 nt in hopes of minimizing the progression to invasive disease.

66 ent cohort with longitudinally monitored pre-invasive disease.

67 risk of recurrence or risk of progression to invasive disease.

68 n early stage before its progression into an invasive disease.

69 ficant disease without occurrences of tissue-invasive disease.

70 els that recapitulate the biology of locally invasive disease.

71 ow they may contribute to the progression to invasive disease.

72 IL-17A neutralization reduced S. pneumoniae invasive disease.

73 er cancers due to frequent recurrence of non-invasive disease.

74 ally prevented from causing acute or chronic invasive disease.

75 nt microbe to bypass host defenses and cause invasive disease.

76 rial pneumonia and otitis media, among other invasive diseases.

77 nd metastatic breast cancers compared to non-invasive diseases.

78 onally breaches epithelial barriers to cause invasive diseases.

79 ntered during infection and establishment of invasive diseases.

80 asionally causes severe and life-threatening invasive diseases.

81 atic adenocarcinomas, with two demonstrating invasive diseases.

82 merge frequently within clinical isolates of invasive diseases.

83 iduals but involved nodes (0.623), and focal-invasive disease (0.727) were included in the definition

84 Serotype III, associated with invasive disease, accounts for 25% (95% CI, 23%-28%), bu

85 f intestinal colonization and progression to invasive disease after postnatal GBS exposure in offspri

86 for CMV disease risk, especially for tissue-invasive disease, after liver transplantation.

87 olonizes the human nasopharynx and can cause invasive disease aided by the pneumococcal capsule.

88 manifestation may range from asymptomatic to invasive disease, amoebic liver abscess being the most c

89 Typhimurium contributes to a high burden of invasive disease among African infants and HIV-infected

90 ed with the observed clinical phenotypes (i) invasive disease and (ii) asymptomatic carriage on the p

91 ate vaccines provide protection against both invasive disease and colonization, but their use in deve

92 ited decreased virulence in a mouse model of invasive disease and decreased multiplication in human b

93 increased in ER+ tumors and associated with invasive disease and distant metastasis.

94 investigations of fundamental mechanisms of invasive disease and evolutionary response.

95 hotype, ST313, was primarily associated with invasive disease and febrile illness.

96 emonstrated less group B streptococcal (GBS) invasive disease and gastrointestinal colonization after

97 r cause of bacteria-associated mortality and invasive disease and is carried asymptomatically by 27%

98 nd used this model to evaluate colonization, invasive disease and natural transformation.

99 emerging both among carriers and as cause of invasive disease and recent studies revealed two main Se

100 reptococcus infection can be associated with invasive disease and severe clinical syndromes, such as

101 virulence may help to improve prediction of invasive disease and suggest new targets for therapeutic

102 imed to examine the current global burden of invasive disease and the serotype distribution of group

103 ed S. pneumoniae from the airway and impeded invasive disease and transmission between mice.

104 utational burden (TMB) was similar to muscle-invasive disease and was highest in GO, intermediate in

105 y S. pneumoniae precedes pulmonary and other invasive diseases and, therefore, is a promising target

106 ence of CMV infection (viremia and/or tissue invasive disease) and risk factors for CMV infection wer

107 asily transmitted, especially prone to cause invasive disease, and infect otherwise healthy individua

108 e explanation for the increased incidence of invasive disease, and rationale for global surveillance.

109 in nasal wash, the incidence of mucosal and invasive disease, and the percentage of contacts that we

110 etics of GBS GI colonization, progression to invasive disease, and the role of GBS-specific IgG produ

111 patients with recurrent, metastatic, or non-invasive disease, and those testing neoadjuvant therapy

112 S. aureus colonization and invasive disease are not associated with the development

113 s of PorB serotypes commonly associated with invasive disease are often conserved, calling into quest

114 termining the development of carriage versus invasive disease are poorly understood but will influenc

115 ococcal progression from this niche to cause invasive disease are poorly understood.

116 d key virulence factors by which SDSE causes invasive diseases are poorly understood.

117 en causing severe local and life-threatening invasive diseases associated with high mortality rates a

118 MV syndrome, and 8 (7%) developed CMV tissue invasive disease at a median of 5.6 months after transpl

119 With the increasing incidence of invasive disease attributed to filamentous fungi, rapid

120 study from the Netherlands, we compared MenC invasive disease between 1998 and the introduction of MC

121 studied for their promising use as minimally invasive disease biomarkers.

122 munication as well as their potential as non-invasive disease biomarkers.

123 fants across the period of susceptibility to invasive disease, but no licensed vaccine exists.

124 reptococcus pneumoniae is a prerequisite for invasive disease, but the majority of carriage episodes

125 Invasive disease caused by drug-resistant strains, desig

126 B is critical for the pathogenesis of severe invasive disease caused by GAS.

127 enB) has been licensed for the prevention of invasive disease caused by MenB.

128 nisation programme in Brazil, PCV10 prevents invasive disease caused by vaccine serotypes.

129 tomatic carriage providing the reservoir for invasive, disease-causing strains.

130 F-kappaB signature response distinct from an invasive-disease-causing isolate of serotype 4 (TIGR4).

131 t on the incidence of CMV syndrome or tissue-invasive disease, chemoprophylaxis was associated with a

132 Isolates from invasive disease contained multiple mutations in the sam

133 Implementation of invasive disease control strategies such as culling may

134 We analyzed pneumococcal carriage and invasive disease data collected from children <7 years o

135 ial pathogen Neisseria meningitidis to cause invasive disease depends on survival in the bloodstream

136 port seven cases of Haemophilus haemolyticus invasive disease detected in the United States, which we

137 ificant increase in the overall incidence of invasive disease-driven primarily by increasing disease

138 Incidence of invasive disease due to H. influenzae serotype a (Hia) i

139 umococcal vaccine use in Mali has diminished invasive disease due to those pathogens.

140 onjunctival nodules but have manifested more invasive disease (eg, spinal, orbital, and subdermal nod

141 oneal fluid of subjects with and without the invasive disease endometriosis.

142 ct infections in children but can also cause invasive disease, especially in older adults.

143 2% in the placebo group (hazard ratio for an invasive-disease event, 0.77; 95% CI, 0.62 to 0.96; P=0.

144 4% in the placebo group (hazard ratio for an invasive-disease event, 1.13; 95% CI, 0.68 to 1.86; P=0.

145 s with microscopically complete excision for invasive disease followed by whole-breast irradiation of

146 At-risk individuals can develop often fatal invasive disease for which therapeutic options are limit

147 EC-T and 82% of those who received ET-X were invasive disease free at 5 years (hazard ratio, 1.30; 95

148 better outcome on adjuvant chemotherapy for invasive disease-free survival (hazard ratio (HR) = 0.42

149 versus the TaxAC regimens was planned, with invasive disease-free survival (IDFS) as the primary end

150 49.6 months (range, 0.5 to 64.0 months), 243 invasive disease-free survival (iDFS) events were report

151 The primary endpoint was invasive disease-free survival (IDFS).

152 ion models stratified by trial were used for invasive disease-free survival (iDFS; primary end point)

153 ons with breast cancer-specific survival and invasive disease-free survival (OS: HR, 0.45; 95% CI, 0.

154 gnificant covariate for overall survival and invasive disease-free survival (P < .001).

155 ase inhibitor, significantly improves 2-year invasive disease-free survival after trastuzumab-based a

156 At 2 year follow-up, 70 invasive disease-free survival events had occurred in pa

157 the neratinib group had significantly fewer invasive disease-free survival events than those in the

158 rapy alone versus chemoendocrine therapy for invasive disease-free survival in women with Oncotype DX

159 The 2-year invasive disease-free survival rate was 93.9% (95% CI 92

160 The 5-year invasive disease-free survival was 90.2% (95% CI 88.3-91

161 Invasive disease-free survival was significantly higher

162 for 12 months significantly improved 2-year invasive disease-free survival when given after chemothe

163 edefined endpoint of the 5-year analysis was invasive disease-free survival, analysed by intention to

164 The primary outcome was invasive disease-free survival, as defined in the origin

165 Invasive disease-free survival, but not OS, was signific

166 or characteristics, and overall survival and invasive disease-free survival.

167 The primary end point was invasive disease-free survival.

168 cific survival: HR, 0.37; 95% CI, 0.15-0.93; invasive disease-free survival: HR, 0.58; 95% CI, 0.34-1

169 s, zoledronic acid was associated with lower invasive-disease-free survival (HR 2.47, 95% CI 1.23-4.9

170 rtuzumab significantly improved the rates of invasive-disease-free survival among patients with HER2-

171 2.0-95.8), MAF status was not prognostic for invasive-disease-free survival in the control group (MAF

172 We assumed a 3-year invasive-disease-free survival rate of 91.8% with pertuz

173 , zoledronic acid was associated with higher invasive-disease-free survival than was control treatmen

174 th node-positive disease, the 3-year rate of invasive-disease-free survival was 92.0% in the pertuzum

175 th node-negative disease, the 3-year rate of invasive-disease-free survival was 97.5% in the pertuzum

176 The estimates of the 3-year rates of invasive-disease-free survival were 94.1% in the pertuzu

177 sease-free survival; the secondary endpoint, invasive-disease-free survival, was the primary disease

178 nce factors promoting Streptococcus pyogenes invasive disease have been described, specific streptoco

179 MV-CD8+ TIC score was associated with tissue-invasive disease (hazard risk, 2.84, 95% confidence inte

180 ypes, and notifications of scarlet fever and invasive disease in 2014-16 using regional (northwest Lo

181 ds has vastly improved knowledge of this new invasive disease in a short time.

182 type 6C, which was described in 2007, causes invasive disease in adults and children.

183 ca serovar Typhimurium, are a major cause of invasive disease in Africa, affecting mainly young child

184 e burden of multidrug-resistant nontyphoidal invasive disease in Africa, escape MAIT cell recognition

185 with gastrointestinal disease worldwide and invasive disease in Africa.

186 ntroduction on pneumococcal colonization and invasive disease in children aged <5 years.

187 meningitidis (MenB) remains a major cause of invasive disease in early childhood in developed countri

188 lacking expression of fHbp and NspA to cause invasive disease in human fH transgenic rats and to surv

189 phtheriae and Corynebacterium ulcerans cause invasive disease in humans and animals.

190 pyogenes (GAS) is a leading cause of severe invasive disease in humans, including streptococcal toxi

191 elations of RASSF1 methylation with advanced invasive disease in humans.

192 ngal infections in immunocompetent hosts and invasive disease in immunocompromised hosts.

193 itis in healthy individuals and for a severe invasive disease in immunocompromised patients.

194 reptococcus pneumoniae is a leading cause of invasive disease in infants, especially in low-income se

195 e-specific capsular antibodies and risks for invasive disease in infants.

196 d nasal neutrophil recruitment and prevented invasive disease in mice.

197 d risk of DCIS recurrence and progression to invasive disease in multivariate analyses.

198 more, NADase activity did not correlate with invasive disease in our collection but was associated wi

199 a commensal and a major pathogen that causes invasive disease in people of all ages.

200 en of group B Streptococcus (GBS), including invasive disease in pregnant and postpartum women, fetal

201 ast but involved nodes (n = 186), only focal-invasive disease in the breast (n = 478), and gross inva

202 complete response, defined as the absence of invasive disease in the breast and axillary lymph nodes,

203 (HER2)-positive breast cancer with residual invasive disease in the breast or axilla after completin

204 ing neonatal pathogen and a growing cause of invasive disease in the elderly, with clinical manifesta

205 s isolates from human patients and pigs with invasive disease in the Netherlands, and validated our o

206 occal transmission as a means of eliminating invasive disease in the population.

207 neonatal gastrointestinal tract and to cause invasive disease in the susceptible neonate.

208 rarely seen in contemporary surveillance of invasive disease in the United States, substantially con

209 Bacterial pathogens that cause invasive disease in the vertebrate host must adapt to ho

210 inhibitor SEL201 blocked DCIS progression to invasive disease in vivo.

211 Kingella kingae is a common cause of invasive disease in young children and was recently foun

212 saccharide vaccine (PPSV23) protects against invasive disease in young healthy persons, randomized co

213 A serocorrelate of protection against invasive disease in young infants is being considered to

214 We compared invasive disease incidence and carriage prevalence befor

215 xplain geographical variation in early-onset invasive disease incidence.

216 Invasive disease includes indolent chronic rhinosinusiti

217 host-defense pathways induced by Spn during invasive disease, including proinflammatory responses an

218 acellular matrix (ECM) are hallmarks of many invasive diseases, including cancer.

219 variety of respiratory infections as well as invasive diseases, including meningitis and sepsis.

220 ensal of the human nasopharynx but can cause invasive diseases, including otitis media, pneumonia, se

221 an opportunistic human pathogen that causes invasive diseases, including pneumonia, with greater hea

222 are present in DCIS before the emergence of invasive disease, indicating that the malignant nature o

223 olic enzymes might play an important role in invasive diseases induced by SDSE.

224 <5 years; years 1997-2000, 2006-2008) and NT invasive disease (IPD) (all ages; years 1994-2007) isola

225 ition of a subset of tumors from indolent to invasive disease is associated with a poor clinical outc

226 st that the frequency of E. coli lineages in invasive disease is driven by negative frequency-depende

227 on the predominant pathogens associated with invasive disease is necessary to inform vaccine prioriti

228 he cho1Delta/Delta mutant's ability to cause invasive disease is severely compromised.

229 d of clinical isolates and more prevalent in invasive disease; it provides genetic diversity and enab

230 y tract infections in children but can cause invasive disease, mainly in older adults.

231 The tendency of S Panama to cause invasive disease may be linked to certain serovar-specif

232 ommon manifestations, but symptoms of tissue invasive disease may be observed.

233 riage (mean pseudo-R2 0.84) and incidence of invasive disease (mean R2 0.89).

234 fficacy was assessed in a skin challenge and invasive disease model.

235 For patients with muscle-invasive disease, more aggressive therapy with radical c

236 the human nasopharynx and skin, also causes invasive disease, most frequently skin and soft tissue i

237 The Streptococcus pneumoniae Invasive Disease network (SpIDnet) actively monitors pop

238 with national increases in scarlet fever and invasive disease notifications, emm1 S pyogenes upper re

239 sheddase activity and cell migration in the invasive disease of endometriosis.

240 healthy children and adults with unexplained invasive disease of the CNS, digestive tract, or both ca

241 adult urogenital tract and are implicated in invasive diseases of adults and neonates.

242 recurrence, or contralateral breast cancer, invasive disease, or ductal carcinoma in situ), analysed

243 characteristics including presence of tissue invasive disease (P<0.05) and increased viral load at ba

244 eus causes many disease syndromes, including invasive disease, pneumonia, and skin and soft tissue in

245 asopharyngeal carriage and serotype-specific invasive disease potential among Native Americans.

246 nd Staphylococcus stand out for their unique invasive disease potential and sophisticated ability to

247 clonal complexes (CCs) showed differences in invasive-disease potential.

248 lso intraclonal variants exhibited different invasive-disease potentials in children.

249 ates representing PFGE clones with different invasive-disease potentials revealed intraclonal sequenc

250 The increase in the NVT invasive disease rate seems to be proportional to the in

251 gen interactions that mediate progression to invasive disease remain unknown due, in part, to a pauci

252 nrelated cocolonizing strains could increase invasive disease risk, and ongoing within-host evolution

253 During both colonization and invasive disease S. pneumoniae ferments host-derived car

254 s tissues (e.g. atrium) and might enable non-invasive disease screening using epigenetic profiles.

255 noninvasive (otitis media and pneumonia) and invasive diseases (sepsis) in humans.

256 Kaplan-Meier estimation was used to compare invasive disease-specific survival rates.

257 e, integrated healthcare system provides non-invasive disease staging and minimizes hepatology clinic

258 lonizer, but can also cause life-threatening invasive diseases such as empyema, bacteremia and mening

259 r lineages but also frequently causes severe invasive disease, such as bacteremia.

260 asive disease was 3-4 times more common than invasive disease, suggesting that adult GBS burden is co

261 coccus (GAS) isolates during a retrospective invasive disease survey in Hawaii.

262 g patients with lung CT scan signs of airway-invasive disease than among other patients (P = .043).

263 MUC1 and is more frequently associated with invasive disease than other IPNB subtypes.

264 cantly more virulent in a mouse model of GAS invasive disease than the wild-type strain.

265 gen Erwinia amylovora causes fire blight, an invasive disease that threatens a wide range of commerci

266 rate of CMV disease (CMV syndrome and tissue-invasive disease that was clinically diagnosed and biops

267 upon deficiencies in the host to facilitate invasive disease, the distinct mechanisms that govern th

268 To understand its potential to cause invasive disease, the genome of Mycoplasma canis strain

269 ningitidis, and Neisseria gonorrhoeae, cause invasive disease: the other eight are carried asymptomat

270 remains the mainstay of treatment for muscle-invasive disease, there is a growing body of evidence su

271 the most common NTS serovars associated with invasive disease, these findings can pave the way for de

272 d S. pneumoniae, which were more virulent in invasive disease, upregulated genes involved in carbohyd

273 idal and nontyphoidal Salmonella serovars to invasive disease varies considerably in place and time,

274 gh CovRS to alter gene expression and reduce invasive disease virulence.

275 Non-invasive disease was 3-4 times more common than invasive

276 The 3-year rate of survival free from invasive disease was 98.7% (95% confidence interval [CI]

277 Invasive disease was defined as GBS isolated from a norm

278 hases') that favour asymptomatic carriage or invasive disease was first reported in 1933.

279 An association of DM with invasive disease was found among transplanted HCC patien

280 eumonia and nasal carriage is a precursor to invasive disease, we explored the role of MIF in the cle

281 IS who are naturally at high risk for future invasive disease were deficient for fetal microchimerism

282 Recurrence patterns of invasive disease were local in 35%, distant in 47%, and

283 iation in IGF1, IGFBP1 or IGFBP3 and risk of invasive disease, whereas five tSNPs in IGF2 were associ

284 dicate with antibiotics than is pneumococcal invasive disease, which may suggest that colonizing pneu

285 hat causes severe local and life-threatening invasive diseases, which are associated with high mortal

286 tions for both nonmuscle-invasive and muscle-invasive disease will enhance our ability to predict whi

287 ingitidis is a major global pathogen causing invasive disease with a mortality of 5-10%.

288 by coupling an epidemiological model of this invasive disease with an opinion dynamics model we are a

289 is responsible for a major global burden of invasive disease with high associated case-fatality rate

290 acellular pathogen capable of causing severe invasive disease with high mortality rates in humans.

291 g challenges the view that PVL mainly causes invasive disease with poor prognosis.

292 e (adenocarcinoma in situ, AIS) to minimally invasive disease with prominent lepidic growth (minimall

293 improve understanding of the epidemiology of invasive disease, with an impact on disease control, not

294 may differ significantly from those causing invasive disease, with PCV7-associated serotypes overrep

295 rsistence, dissemination, and development of invasive disease within an individual human host.

296 ive: To investigate the occurrence of occult invasive disease within in situ melanoma by using method

297 ent nonlepidic growth component representing invasive disease within individual tumors.

298 ortant cause of intrapulmonary infection and invasive disease worldwide.

299 occus (GBS) is the leading cause of neonatal invasive disease worldwide.

300 uired for both asymptomatic colonization and invasive disease, yet the expression level is different