ライフサイエンスコーパス: severe disease

1 s from 0 to 12 (0 = no disease and 12 = most severe disease).

2 d mild to moderate disease and 171 [20%] had severe disease).

3 0 to 176, with higher scores signifying more severe disease).

4 (healthy, mild periodontitis, or moderate-to-severe disease).

5 rs of age, but only a subset of children get severe disease.

6 9%) developed moderate disease and 48 (4.3%) severe disease.

7 ividuals with COVID-19 experiencing mild and severe disease.

8 egulated inflammation in causing age-related severe disease.

9 ks the systemic inflammation of moderate and severe disease.

10 ow absolute numbers are associated with very severe disease.

11 oidosis may be an additional risk factor for severe disease.

12 gal involvement in asthma is associated with severe disease.

13 only fungal, is more common in patients with severe disease.

14 e, and golden hamsters, which may model more severe disease.

15 as a post-exposure therapy to limit or treat severe disease.

16 cy at preventing Covid-19 illness, including severe disease.

17 t and hospitalized US Veterans, resulting in severe disease.

18 l as composite symptoms associated with more severe disease.

19 us and a major public health concern causing severe disease.

20 %) had mild, 41 (46%) moderate, and 27 (30%) severe disease.

21 cross the epithelial barrier and cause more severe disease.

22 discriminated between patients with mild and severe disease.

23 d a relatively short follow-up or focused on severe disease.

24 c origin were identified as risk factors for severe disease.

25 ty, pandemic potential, and ability to cause severe disease.

26 factors for RSV infection and progression to severe disease.

27 asthma, but it is particularly prevalent in severe disease.

28 anti-CD20 antibody rituximab in moderate and severe disease.

29 olerae, is required for V. cholerae to cause severe disease.

30 ct humans, with IAV and IBV causing the most severe disease.

31 herapeutic targets for the treatment of this severe disease.

32 se vaccine recipients were protected against severe disease.

33 6.6 million meeting criteria for moderate to severe disease.

34 , and these patients are older and have more severe disease.

35 gs present a possible treatment modality for severe disease.

36 mic infection was the strongest predictor of severe disease.

37 c factors, with higher heritability for more severe disease.

38 ecting humans, which results in mild to very severe disease.

39 luding decreased pulmonary function and more severe disease.

40 fy them as a potential target for preventing severe disease.

41 was identified as a significant predictor of severe disease.

42 t agents with the potential to rapidly cause severe disease.

43 ctively) and were significantly increased in severe disease.

44 e significant human pathogens that can cause severe disease.

45 t higher risk for liver involvement and more severe disease.

46 d biomarkers that detect patients at risk of severe disease.

47 phisms that confer innate protection against severe disease.

48 hought to be responsible for the symptoms of severe disease.

49 ry diseases outcomes cohort, of whom 595 had severe disease.

50 olar lavage fluid mitochondrial DNA and more severe disease.

51 normal RPGR allele was associated with more severe disease.

52 d patients is critical for the prevention of severe disease.

53 tokine homolog, a virulence factor linked to severe disease.

54 fections(14,15), and these children had more severe disease.

55 were classified as having either minimal or severe disease.

56 variant in RPGRIP1L was associated with more severe disease.

57 gely restricted to patients with moderate-to-severe disease.

58 rom healthy controls and to predict mild and severe disease.

59 are highly effective therapy for moderate-to-severe disease.

60 subjects (43%) and was associated with more severe disease.

61 s to both viral clearance and progression to severe disease.

62 pathogenesis, particularly in patients with severe disease.

63 number of sequence variants, some can cause severe diseases.

64 ificant clinical impact for the treatment of severe diseases.

65 rcent of asthmatics have what is considered "severe" disease.

66 In eyes with severe disease, 31.6% were classified as progressing at

67 ren aged >18 months were less likely to have severe disease (9%; 5 of 56) than unvaccinated children

68 of 99.4% and 86.3%, being 40.3% and 33.8% of severe disease according to 2017-WW and CDC/AAP case def

69 id not differ between patients with mild and severe disease according to Ranson and APACHE II scores.

70 Patients with severe disease according to Ranson's Criteria (n = 24) h

71 ranges from 1 (no disease activity) to 100 (severe disease activity).

72 C) present with, or progress to, moderate to severe disease activity.

73 Challenges to the prevention of severe disease after virus infection include both a pauc

74 Infants with moderate-severe disease also had increased shunt.

75 ients with hypertension or with mortality or severe disease among patients diagnosed as having COVID-

76 part by concerns of disproportionately more severe disease among solid organ transplant (SOT) recipi

77 mately 20% of patients with COVID-19 develop severe disease and 5% of patients require intensive care

78 lial glycocalyx breakdown is associated with severe disease and a fatal outcome in adults with falcip

79 igher baseline ONSD was associated with more severe disease and abnormal brain imaging (abnormal imag

80 ss of transitional and follicular B cells in severe disease and accumulation of SARS-CoV-2-specific "

81 d infection with ribotype 027 associate with severe disease and adverse outcomes.

82 s that are associated with increased risk of severe disease and are nonredundant or redundant for pro

83 he mechanisms that underlie the male bias in severe disease and death from coronavirus disease 2019 (

84 ical conditions are at much greater risk for severe disease and death from Covid-19 infection.

85 Males are disproportionately affected by severe disease and death from severe acute respiratory s

86 s (aged >=70 years) are at increased risk of severe disease and death if they develop COVID-19 and ar

87 virus 2 (SARS-CoV-2) or increase the risk of severe disease and death upon infection.

88 iovascular disease have an increased risk of severe disease and death.

89 The studies of MERS patients with severe disease and experimentally infected animals showe

90 en is critical for preventing progression to severe disease and for reducing the continued high burde

91 ients with bronchiectasis in India have more severe disease and have distinct characteristics from th

92 cluding Ebola and Marburg viruses, can cause severe disease and high mortality rates on spillover int

93 ng, not recruiting), adults with moderate to severe disease and inadequate control by topical treatme

94 pper reference limit and are associated with severe disease and increased inflammatory markers.

95 eat-tested patients were more likely to have severe disease and low viral loads.

96 We observed high rates of severe disease and mortality in our hospitalized patient

97 Risk factors associated with severe disease and mortality include advanced age, hyper

98 children, because of their increased risk of severe disease and mortality.

99 highly pathogenic human coronavirus causing severe disease and mortality.

100 s (cholelithiasis) is a highly prevalent and severe disease and one of the leading causes of hospital

101 alternative disease paths that lead to more severe disease and poorer outcomes.

102 lunteers with this live virus risks inducing severe disease and possibly even death.

103 nowledge of biomarkers to objectively define severe disease and predict clinical outcomes.

104 She developed severe disease and rapid viral dissemination that elicit

105 ith greater genetic diversity can cause more severe disease and stimulate antibody responses with red

106 At present, predictors of severe disease and the efficacy of different treatments

107 e ability of HPAI H7N9 viruses to cause more severe disease and to replicate in brain tissues in anim

108 m COVID-19 (28 with mild disease and 14 with severe disease) and 16 unexposed donors, using interfero

109 sease, 17 with moderate disease, and 24 with severe disease) and 20 healthy subjects.

110 b) SARS-CoV-2 persisted longer in those with severe disease, and (c) there was cross-reactivity betwe

111 (9,778 malaria patients, including 343 with severe disease, and 674 healthy participants) from 43 st

112 e therapy at diagnosis or at early stages of severe disease, and for patients failed by steroid and i

113 titers in these assays associated with more-severe disease, and no cross-reactive Abs against prior

114 y enterovirus A71 (EV-A71), presents mild to severe disease, and sometimes fatal neurological and res

115 0 to 12, with higher scores indicating more severe disease] and no subscore >1 [range, 0 to 3] on an

116 0 to 12, with higher scores indicating more severe disease] and no subscore >1 [range, 0 to 3] on an

117 Here, we develop novel severe-disease animal models for COVID-19 involving disr

118 glaucomatous eyes with early, moderate, and severe disease (ANOVA and linear regressions of thicknes

119 Some histoplasmosis patients experienced severe disease, apparent diagnostic delays, and prolonge

120 ations, host genetic factors associated with severe disease are largely unknown.

121 models of SARS-CoV-2 infection that manifest severe disease are needed to investigate the pathogenesi

122 man host that lead to asymptomatic, mild, or severe disease are poorly understood, in part, because l

123 9 patients, we demonstrate that moderate and severe disease are separated by specific differences in

124 restrict viral propagation and protect from severe disease are unclear.

125 ecipients, who are at presumed risk for more severe disease, are not well characterized.

126 itulating human COVID-19 disease, especially severe disease, are urgently needed to understand pathog

127 sed likelihood of VA treatment included more severe disease as indicated by recent right heart failur

128 ion and simultaneously promote recovery from severe diseases associated with respiratory viral infect

129 Patients present with severe disease at a relatively early age and most (67%)

130 previously showed were elevated in moderate/severe disease at baseline, 24 had statistically signifi

131 th IBS-C (Rome III criteria) and moderate to severe disease at inclusion (IBS Symptom Severity Scale

132 in IBD are associated with inflammation and severe disease, but normalized after anti-cytokine thera

133 hypertension are risk factors for developing severe disease, but so far immunosuppressed patients who

134 development has been slow for this typically severe disease, but there is current optimism for curati

135 1-unit increase in CRP increased the risk of severe disease by 0.06%.

136 mong PCR(+)/EIA(-) patients include baseline severe disease by IDSA criteria, baseline fulminant coli

137 iable logistic regression analyses, baseline severe disease by Infectious Diseases Society of America

138 While symptoms are generally mild, severe disease cases have been reported, but knowledge o

139 The reasons for the enhanced spread and severe disease caused by newly emerging strains are not

140 COVID-19 is a potentially severe disease caused by the recently described SARS-CoV

141 ug or vaccine has been approved to treat the severe disease caused by this coronavirus, COVID-19.

142 Yellow Fever (YF) is a severe disease caused by Yellow Fever Virus (YFV), endem

143 Severe disease centers on older persons with preexisting

144 CHIKV causes chikungunya fever, a mild to severe disease characterized by arthralgia, with some fa

145 comes as all-cause mortality, progression to severe disease, clinical symptoms, and upper respiratory

146 y higher in nasal aspirates of patients with severe disease compared with those of patients with mode

147 pothesized absence of enFeLV results in more severe disease consequences in felid species lacking the

148 ic diseases, resulting in more patients with severe disease considering pregnancy.

149 RV infection was also associated with more severe disease course during the 12-month follow-up in t

150 he T allele of rs8005161 might confer a more severe disease course in IBD patients.

151 ever, among the 6.4% of patients with SLI, a severe disease course should be anticipated.

152 and that mice lacking Slc7a2 exhibit a more severe disease course when exposed to dextran sulfate so

153 ared between patients with mild/moderate and severe disease (defined as ICU admission, intubation or

154 dy involving 1980 patients with Covid-19 and severe disease (defined as respiratory failure) at seven

155 e number of individuals at increased risk of severe disease (defined as those with at least one condi

156 We evaluated individuals with and without severe disease, defined as admission to the intensive ca

157 ome profiles and their association with more-severe disease, defined by use of positive pressure vent

158 d to model the relative increase of risk for severe disease, depending on the measured densities.

159 -infected pediatric patients correlates with severe disease development.

160 More severe disease develops in a few models, some associated

161 Patients with severe disease display excessive neutrophil extracellula

162 Metabolic syndrome increases the risk of severe disease due to viral infection.

163 en vaccinated might be at risk of developing severe disease during a subsequent exposure to wild-type

164 Since this case, any patient with severe disease (eg, ARDS or pneumonia) requiring hospita

165 to distinguish non-specific complications of severe disease (eg, hypoxic encephalopathy and critical

166 ratures is often predicted to result in more severe disease epidemics.

167 Frequent reactivation has been linked to severe diseases, especially in immunocompromised individ

168 ease 2019 (COVID-19) cases, individuals with severe disease exhibited elevated virus-neutralizing tit

169 CD8+ T cells in patients with severe disease express high levels of cytotoxic molecule

170 e inversions, transient QT prolongation, and severe disease expression of exercise-induced cardiac ar

171 tive humidity makes mice more susceptible to severe disease following respiratory challenge with infl

172 Severe disease following respiratory syncytial virus (RS

173 the increased likelihood of developing more severe disease from Chlamydia infection.

174 eas the profiles of those with who developed severe disease had elevated levels of all four signature

175 s with atopic dermatitis and those with more severe disease had higher scores in the dermatology life

176 Measurements and Main Results: Patients with severe disease had increased proportions of CD8 (cluster

177 Nasal aspirates from patients with severe disease had reduced concentrations of IL-17.

178 Severe disease has been associated with changes in perip

179 cation of immune correlates of protection or severe disease have challenged the development and evalu

180 In another paradigm of receptor-facilitated severe disease, henipaviruses, including Nipah and Hendr

181 iduals are at particular risk for developing severe disease; however, no approved antiviral therapies

182 cal chaperones that target FAH to tackle the severe disease HT1.

183 to vancomycin in vitro and resulted in more severe disease in a humanized mouse model.

184 leishmaniasis (Leishmania donovani) but more severe disease in a model of malaria (Plasmodium chabaud

185 SARS-CoV-2 MA caused more severe disease in aged mice, and exhibited more clinical

186 HeV) are zoonotic paramyxoviruses that cause severe disease in both animals and humans.

187 Cytomegalovirus (CMV) can cause severe disease in children and adults with a variety of

188 Influenza B virus (IBV) infections can cause severe disease in children and the elderly.

189 to clonal group CG258, is capable of causing severe disease in humans and is classified as an urgent

190 of pathogens that are implicated in mild to severe disease in humans and other animals.

191 MARV causes severe disease in humans with high fatality.

192 h severe LF.IMPORTANCE Lassa fever may cause severe disease in humans, in particular in areas of ende

193 Virus infection can result in severe disease in humans, including microcephaly in newb

194 rus (ZIKV) is a global health threat causing severe disease in humans, including microcephaly in newb

195 ighly pathogenic zoonotic viruses that cause severe disease in humans.

196 d some, such as H5N1 and H7N9 viruses, cause severe disease in humans.

197 lities in congenitally infected children and severe disease in immunocompromised patients.

198 Human cytomegalovirus (HCMV) causes severe disease in infants and immunocompromised people.

199 ung and airway neutrophils are a hallmark of severe disease in infants with respiratory syncytial vir

200 ed in the mid- to late 1990s in outbreaks of severe disease in livestock and people in Australia and

201 us (CMV) is a herpesvirus capable of causing severe disease in neonates and immunocompromised patient

202 ociation between body mass index and risk of severe disease in patients with coronavirus disease 2019

203 (hTR), but these effects do not explain the severe disease in patients.

204 H5 A/goose/Guangdong/1/96 lineage can cause severe disease in poultry and wild birds, and occasional

205 SARS-CoV-2 infection causes more severe disease in pregnant women compared to age-matched

206 e show that infection with SARS-CoV-2 causes severe disease in the lung and, in some mice, the brain.

207 um and the causative agent of melioidosis, a severe disease in tropical regions.

208 virus (CPV) is an important pathogen causing severe diseases in dogs, including acute hemorrhagic ent

209 pper homeostasis leads to the development of severe diseases in humans.

210 Further notable predictors of severe disease included having neural and/or renal tropi

211 ulations and cause a spectrum of potentially severe diseases including hepatitis, vascular shock synd

212 and mutations impairing their activity cause severe diseases, including campomelic dysplasia (SOX9),

213 some of the infections being associated with severe disease, indicates that ICV infection has the pot

214 necessary diagnostic tests, risk factors for severe disease, indicators for hospital admission, disch

215 human viruses, which could contribute to the severe disease induced by avian IAV in humans.IMPORTANCE

216 Moderate-severe disease is associated with a high incidence of pu

217 ibution of treatment delay on progression to severe disease is critical to determine how quickly pati

218 trategy for hrTA-TMA, but some patients with severe disease lacked a complete response, prompting us

219 omorbidities because they are likely to have severe diseases leading to hospitalization and surgical

220 F8-/-mice or PN-1 blocking in patients with severe disease led to a significantly improved thrombin

221 ls are thought to be at an increased risk of severe disease, little is known about their clinical pre

222 st that aged AGMs may be useful for modeling severe disease manifestations, including ARDS.

223 Patients in the n-FP access group had more severe disease (mean logistic EuroSCORE 19.95 vs. 16.95;

224 VID-19) and (2) risk factors predisposing to severe disease/mortality in the general population also

225 Patients with severe disease (n = 38) develop a robust antibody respon

226 ved in both survivors and non-survivors with severe disease, non-survivors showed attenuated IgG resp

227 rhesus macaque model does not represent the severe disease observed in some patients with COVID-19,

228 Severe disease occurred in 49%.

229 and were independently associated with more severe disease (odds ratio = 3.2; 95% confidence interva

230 Fusarium head blight (FHB) is a severe disease of wheat (Triticum aestivum L.).

231 Most cases are mild; severe disease often involves cytokine storm and organ f

232 on of coronavirus disease 2019 (COVID-19) to severe disease or death are underexplored in U.S. cohort

233 imary outcomes were death and a composite of severe disease or death.

234 to moderate disease, 302 (38%) progressed to severe disease or death: 181 (60%) by day 2 and 238 (79%

235 uired to assess the role of typhoid toxin in severe disease or the establishment of bacterial carriag

236 ty in humans from the milder dengue fever to severe disease, or dengue hemorrhagic fever (DHF).

237 dysfunctional T cell responses correlate to severe disease outcomes during human WNV infection.

238 is the subtype most commonly associated with severe disease outcomes such as hemorrhagic colitis and

239 iated viremia is a prerequisite for the most severe disease outcomes, abortion and equine herpesvirus

240 d the potential involvement of TREM-1 in the severe disease pathogenesis, thus providing new insights

241 ilure to form the NSC in FOP results in more severe disease pathology.

242 All cases presented with severe disease, predominantly miliary TB (n = 14; 78%).

243 All cases presented with severe disease, predominately miliary TB (n=14;78%).

244 Severe disease presented with widespread chorioretinal a

245 ers found that (a) individuals with mild and severe disease produced neutralizing IgG to SARS-CoV-2 1

246 viously identified as major risk factors for severe disease progression in COVID-19.

247 ung density measurements to predict possible severe disease progression in COVID-19.

248 cal disease, role in transmission, risks for severe disease, protective immunity, as well as novel th

249 Hia infection can cause severe disease requiring hospitalization and may also ca

250 nd how these responses may contribute to the severe disease seen in CCHFV-infected humans in order to

251 nse to the intervention between moderate and severe disease severity groups.

252 Mice infected with SKE developed less severe disease signs, including diminished swelling in t

253 ion in AMD, but only in patients with a less severe disease stage.

254 rovement, as measured by the CGI-I, and less severe disease states, as measured by the CGI-S.

255 e harmless, some of them are responsible for severe diseases such as AIDS, viral hepatitis, and flu.

256 ne biomarkers which are associated with some severe diseases such as cancers.

257 an important pathogen in horses that causes severe diseases such as pneumonia and abortion.

258 ssion, frequent HSV-1 reactivation can cause severe diseases, such as blindness and encephalitis.

259 colonize the female genital tract and cause severe diseases, such as puerperal sepsis, neonatal infe

260 sity was associated with an elevated risk of severe disease, suggesting an epistatic relationship bet

261 lial HCM in childhood is varied and includes severe disease, suggesting that clinical screening shoul

262 In 5 patients with early onset and severe disease, survival and motor functions were better

263 phorylation of HSP90 is sufficient to induce severe disease symptoms in plants infected with the bact

264 ow that H304R/R mice have significantly more severe disease symptoms than the heterozygous H304R/+mic

265 Ciliary dysfunction causes severe diseases, termed ciliopathies.

266 bowel disease (IBD) is believed to be a more severe disease than adult-onset IBD, but there is little

267 nt and stabilisation that are more marked in severe disease than in mild disease.

268 The M+ group displayed more severe disease than the M- group, with a greater frequen

269 diagnosed plus disease in patients with less severe disease than the other examiners (P < 0.01).

270 WHO as a priority pathogen because it causes severe disease that has a high mortality rate, epidemic

271 d symptoms of short duration, others develop severe disease that leads to acute respiratory distress

272 cardiopulmonary disease are risk factors for severe disease, the majority of infants hospitalized wit

273 type 2 (Th2) cell pathology is implicated in severe disease, the mechanisms underlying the developmen

274 utilized to differentiate patients prone to severe disease, thereby facilitating earlier implementat

275 Psoriatic arthritis (PsA) is the most common severe disease thought to cause dactylitis.

276 also been implicated in the pathogenesis of severe disease through production of damaging inflammato

277 domestic carnivores, which are vulnerable to severe disease under certain circumstances.

278 and antibody responses are believed to cause severe disease upon respiratory virus infections.

279 verall, and possibly better efficacy in more severe disease warrant further study.

280 er CD4+ T-cell suppression in the context of severe disease was due to the extracellular adenosine ac

281 Risk of symptomatic DENV2 infection and severe disease was elevated by one prior ZIKV infection,

282 OG(35-55), where lack of B cells yields more severe disease, we show here that the immunodominant mye

283 In influenza patients with moderate-to-severe diseases, we uncover a complex landscape of immun

284 Viral load at presentation and the odds of severe disease were highest among patients with low to i

285 CIs) were predictors for hospitalization and severe disease, whereas receipt of chemotherapy and majo

286 apid access to treatment and reduced risk of severe disease, which was particularly strong for SMA.

287 mained unanswered: why some patients develop severe disease, while others do not; and what roles do g

288 ition to protecting those at highest risk of severe disease) will likely be critical to stem the pand

289 nsis causes pneumonic tularemia in humans, a severe disease with a 30 to 60% mortality rate.

290 CHP is a severe disease with a bad mid-term prognosis.

291 dietary intake potentiates RSV infection and severe disease with associated mitochondrial metabolic d

292 However, these infections may progress to severe disease with different clinical manifestations.

293 Yet, these patients had severe disease with elevated inflammatory biomarkers, mu

294 ssemination beyond the respiratory tract, to severe disease with fatal outcome.

295 Acute kidney injury is a severe disease with high morbidity and mortality.

296 ility Facial Anomalies (ICF) 4 syndrome is a severe disease with increased mortality caused by mutati

297 oding the VGSC beta1 subunits, are linked to severe diseases with high risk for sudden death, includi

298 KO (recipient) chimeric mice exhibited more severe disease, with an enhanced Ifn-gamma signature and

299 erate disease, whereas 39 patients (52%) had severe disease, with no ocular involvement in any patien

300 treatment-seeking pathways to hospitals for severe disease would improve our understanding of catchm