ライフサイエンスコーパス: invasive disease

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

2 h generally lacked the genes associated with invasive disease.

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

4 oad-spectrum efficacy against staphylococcal invasive disease.

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

6 ithelial neoplasia after exclusion of occult invasive disease.

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

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

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

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

11 evels of capsule to promote colonization and invasive disease.

12 re the most common serotypes associated with invasive disease.

13 olonization but a higher propensity to cause invasive disease.

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

15 found in blood specimens from patients with invasive disease.

16 ht mechanisms whose perturbation may lead to invasive disease.

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

18 of genes typically involved in localized and invasive disease.

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

20 with both host and pathogen determinants of invasive disease.

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

22 high rates of pneumococcal colonization and invasive disease.

23 sue infections and are comparatively rare in invasive disease.

24 nous dissemination in compromised hosts with invasive disease.

25 ally prevented from causing acute or chronic invasive disease.

26 ow this important human pathogen establishes invasive disease.

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

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

29 ci disseminate from the nasopharynx to cause invasive disease.

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

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

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

33 both commensalism and dissemination to cause invasive disease.

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

35 gram is relevant to malignant progression in invasive disease.

36 phagocytic clearance more effectively during invasive disease.

37 increased neutrophils in the airway and more invasive disease.

38 No unique patterns were associated with invasive disease.

39 aryngeal colonization but did not affect GAS invasive disease.

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

41 oportions of various Candida species causing invasive disease.

42 so decreased among those with hospital-onset invasive disease.

43 lie selection for characteristics that allow invasive disease.

44 ce-associated protein A was linked only with invasive disease.

45 s the gold standard for management of muscle invasive disease.

46 bsence of SpeB production is associated with invasive disease.

47 fficient to prevent conidial germination and invasive disease.

48 OR inhibition for treatment of patients with invasive disease.

49 novial cells and are selected against during invasive disease.

50 ipates in the transition from preinvasive to invasive disease.

51 e with tumor progression from superficial to invasive disease.

52 red for transmission of the bacteria and for invasive disease.

53 e studied, of which 129 were associated with invasive disease.

54 lones to cause local (e.g., otitis media) or invasive disease.

55 spiratory tract, but also occasionally cause invasive disease.

56 arasite Entamoeba histolytica do not develop invasive disease.

57 nd is an important cause of otitis media and invasive disease.

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

59 cal nasopharyngeal carriage to pneumonia and invasive disease.

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

61 rrelated with susceptibility to neonatal GBS invasive disease.

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

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

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

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

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

67 d disease severity and persistence following invasive disease.

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

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

70 d calponin expression on DCIS progression to invasive disease.

71 differentiation occurs before transition to invasive disease.

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

73 onally breaches epithelial barriers to cause invasive diseases.

74 ntered during infection and establishment of invasive diseases.

75 asionally causes severe and life-threatening invasive diseases.

76 atic adenocarcinomas, with two demonstrating invasive diseases.

77 ing from localized respiratory infections to invasive diseases.

78 merge frequently within clinical isolates of invasive diseases.

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

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

81 0001), reducing the incidence of ipsilateral invasive disease (0.32, 0.19-0.56; p<0.0001) as well as

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

83 =0.005), but having no effect on ipsilateral invasive disease (0.95, 0.66-1.38; p=0.8).

84 With respect to invasive disease, 13 serotypes had a significantly highe

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

86 tial morbidity and mortality associated with invasive disease, adolescent health providers must be fa

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

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

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

90 gate vaccine (PCV7) resulted in decreases in invasive disease among children and elderly persons.

91 ight delay detection of inadequately treated invasive disease and because the effectiveness of additi

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

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

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

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

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

97 icates that manganese efflux is required for invasive disease and may provide a useful antimicrobial

98 vasive to invasive) melanoma is required for invasive disease and metastasis.

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

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

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

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

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

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

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

109 NP carriers with five 6A strains that caused invasive disease, and we observed less C3 ( approximatel

110 at bacteria isolated from the sites of human invasive disease are almost invariably monoclonal.

111 e critical interactions with the host during invasive disease are likely to be secreted.

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 fe threatening, and 30% presenting as muscle-invasive disease associated with a high risk of death fr

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

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

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

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

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

123 up C and G streptococci cause a considerable invasive disease burden and sometimes cause disease outb

124 Invasive disease but not colonization elicits beta C-spe

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

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

127 ae are established as virulence features for invasive disease, but their role in respiratory tract in

128 Invasive disease caused by drug-resistant strains, desig

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

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

131 ent gene regulatory system contribute to the invasive diseases caused by group A Streptococcus (GAS).

132 s aureus pneumonia is one of the most common invasive diseases caused by this human pathogen.

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

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

135 collection of MRSA isolates associated with invasive disease, collected in 2005 and 2006 in the Unit

136 Isolates from invasive disease contained multiple mutations in the sam

137 Muscle invasive disease continues to be managed by radical cyst

138 Implementation of invasive disease control strategies such as culling may

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

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

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

142 nt during the transition from preinvasive to invasive disease, distinct molecular alterations are obs

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

144 Invasive disease due to Acinetobacter baumannii is an in

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

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

147 GAS315 (a serotype M3 strain associated with invasive disease) encodes a proline at amino acid positi

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

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

150 2% in the placebo group (hazard ratio for an invasive-disease event, 0.77; 95% CI, 0.62 to 0.96; P=0.

151 4% in the placebo group (hazard ratio for an invasive-disease event, 1.13; 95% CI, 0.68 to 1.86; P=0.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 2.0-95.8), MAF status was not prognostic for invasive-disease-free survival in the control group (MAF

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

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

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

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

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

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

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

180 rmally commensal bacteria occasionally cause invasive disease: host susceptibility, stochasticity in

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

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

183 with gastrointestinal disease worldwide and invasive disease in Africa.

184 and 2004-2006, there was an 82% increase in invasive disease in Alaska Native children younger than

185 not only effective against invasive and non-invasive disease in all ages but also has a significant

186 type 19A has become the predominant cause of invasive disease in children.

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

188 nes of A. baumannii are more likely to cause invasive disease in hospitalized patients is unknown.

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

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

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

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

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

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

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

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 roup B Streptococcus (GBS) is major cause of invasive disease in newborn infants and the leading caus

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

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

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

202 amatic increase in reports of NTS-associated invasive disease in sub-Saharan Africa.

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

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

205 sponse (pCR) rate, defined as the absence of invasive disease in the breast and axillary nodes.

206 he treated group versus 7 of 20 animals with invasive disease in the control group; P = 0.017) and pr

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

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

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

210 r nerve tumor invasion (1 of 20 animals with invasive disease in the treated group versus 7 of 20 ani

211 The management of muscle invasive disease in the United States centers on radical

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

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

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

215 We compared invasive disease incidence and carriage prevalence befor

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

217 Invasive disease includes indolent chronic rhinosinusiti

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

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

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

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

222 <5 years; years 1997-2000, 2006-2008) and NT invasive disease (IPD) (all ages; years 1994-2007) isola

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

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

225 occi that can escape serum killing and cause invasive disease is of concern for future vaccination st

226 The gold standard for management of muscle invasive disease is radical cystectomy.

227 The standard of care for muscle-invasive disease is radical cystoprostatectomy, and seve

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

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

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

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

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

233 fold attenuation in virulence in a zebrafish invasive-disease model.

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

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

236 accines (PCVs) prevent vaccine serotype (VT) invasive disease; nonvaccine serotype (NVT) disease incr

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

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

239 Endemic and epidemic shigellosis, an acute invasive disease of the lower intestines, afflicts milli

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

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

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

243 ial factor in GBS intracellular survival and invasive disease pathogenesis.

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 iliense from isolates from two patients with invasive disease representing the first reported cases i

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 -8 and its activity is associated with human invasive disease severity.

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

257 us genotypes exhibited the capacity to cause invasive disease, strains within CC5 and CC30 exhibited

258 S. pneumoniae causes invasive diseases such as pneumonia, meningitis, and oti

259 n certain patient populations, VGS can cause invasive disease, such as endocarditis, intra-abdominal

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

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

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

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

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

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

266 ity from self-limiting pharyngitis to severe invasive diseases that are associated with significant m

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

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

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

272 meningitis and non-pneumonia, non-meningitis invasive disease using disease incidence and case-fatali

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

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

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

278 kingae type IV pili during colonization and invasive disease, we examined a collection of clinical i

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

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

281 Cases of invasive disease were identified in 8 geographic areas t

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

283 ative) neisserial isolates from persons with invasive disease, where the bacteria encounter high leve

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

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

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

287 Both cell types play a role in invasive disease: while hyphal and pseudohyphal filament

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

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

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

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

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

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

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

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

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

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

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

299 ortant cause of intrapulmonary infection and invasive disease worldwide.

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