ライフサイエンスコーパス: severe infection

1 ce treatment for young infants with clinical severe infection.

2 -threatening inflammatory response caused by severe infection.

3 tion within the human body may contribute to severe infection.

4 o animal studies on the role of platelets in severe infection.

5 and 0.54 (95% CI, 0.33-0.88; P = 0.013) for severe infection.

6 mediated antiviral pathways and apoptosis in severe infection.

7 cules in the blood of patients with mild and severe infection.

8 nd their release into circulation induced by severe infection.

9 ve 60 were significantly more likely to have severe infection.

10 sociated immune suppression in patients with severe infection.

11 icipants fulfilled prespecified criteria for severe infection.

12 ism risk evaluation similar to any acute and severe infection.

13 drome involving complications as a result of severe infection.

14 ssociated with protection against common and severe infection.

15 LRP3-induced necrosis in the pathogenesis of severe infection.

16 wn about the mechanisms of susceptibility to severe infection.

17 COVID-19 pneumonia in patients with no prior severe infection.

18 fficient to provide benefit in management of severe infection.

19 compromised neutrophil recruitment, and more-severe infection.

20 ated with greater T cell exhaustion and more severe infection.

21 s is characterized by a systemic response to severe infection.

22 in either group experienced a severe or very severe infection.

23 Coccidioidomycosis ranges from a mild to a severe infection.

24 ng to inflammation that may enhance risk for severe infection.

25 Patients with suspected severe infection.

26 generates local inflammation as a feature of severe infection.

27 ckade as a potential therapeutic modality in severe infection.

28 mmunity health worker with signs of clinical severe infection.

29 in intensive care units is sepsis caused by severe infection.

30 idase levels in the airway are indicative of severe infection.

31 g possible immuno-pathogenetic mechanisms of severe infection.

32 V+ T cells might represent a novel marker of severe infection.

33 s of enterovirus infection in mice, not just severe infections.

34 contaminated water can lead to outbreaks and severe infections.

35 ency that causes increased susceptibility to severe infections.

36 ty and shock in critically ill patients with severe infections.

37 rade 4 hematologic toxicity and 6 documented severe infections.

38 ngers as potential adjuvant therapies during severe infections.

39 an pathogen that can cause two categories of severe infections.

40 lize different virulence mechanisms to cause severe infections.

41 e of solid organ tumor and opportunistic and severe infections.

42 e development and function and presents with severe infections.

43 e vital for controlling viral replication in severe infections.

44 ients with urosepsis than in those with less severe infections.

45 n damage and improves animal survival during severe infections.

46 cated in contributing to the pathogenesis of severe infections.

47 ce factor for Staphylococcus aureus to cause severe infections.

48 address the high rate of relapse and risk of severe infections.

49 verity, with pneumonia being one of the most severe infections.

50 cal devices are increasingly associated with severe infections.

51 lung diseases, Pandoraea species can produce severe infections.

52 nonmyeloablative and was not associated with severe infections.

53 ells, leading to increased susceptibility to severe infections.

54 ely evaluated 294 patients with moderate and severe infections.

55 atment and reduce risks of recurrent or more severe infections.

56 increased susceptibility to recurrent and/or severe infections.

57 nodeficiency virus (HIV) have a high risk of severe infections.

58 crobiota far more frequently than they cause severe infections.

59 nually and over half a million deaths due to severe infections(1).

60 Incidence of severe infection 10 years after transplantation was high

61 renal transplantation, 14 patients developed severe infections (16 bacterial, 4 viral, 1 parasitic).

62 with myocardial infarction); 51 (46.4%) had severe infections (21.8% with H1N1); electrolyte disturb

63 ath are estimated to be preterm birth (28%), severe infections (26%), and asphyxia (23%).

64 anding of the complex biological response to severe infection, a problem of growing magnitude in huma

65 loping in the lung after the resolution of a severe infection acquire tolerogenic properties that con

66 Sepsis, a condition caused by severe infections, affects more than 30 million people w

67 mmune dysfunction contributes to the risk of severe infections after allogeneic hematopoietic stem ce

68 al clinical applications of M-CSF to prevent severe infections after HS/PC transplantation.

69 The increased risk of mortality and severe infections after incidental splenectomy should be

70 on, relapse, death, allergy to rituximab, or severe infection) after transplantation among patients w

71 ctor, and it provides 75% protection against severe infection and 80% protection against death for bo

72 on model, HlaH35L immunization led to a less severe infection and decreased S. aureus levels at the c

73 on that represents a patient's response to a severe infection and has a very high mortality rate.

74 ns in individuals suffering from moderate or severe infection and in individuals who recovered from m

75 with a lower rate of virus clearance in the severe infection and is partially regulated by the expre

76 te individuals at risk of the development of severe infection and predict disease outcome.

77 onal influenza epidemics lead to 3-5 million severe infections and 290,000-650,000 annual global deat

78 However, we observed a high degree of severe infections and an unexpected high number of SPMs,

79 n disseminate from the lungs to the heart in severe infections and can induce cardiac pathology, but

80 patients at an increased risk of developing severe infections and cancer.

81 CTs) that can help to identify children with severe infections and children in need of antibiotic tre

82 yelitis using IDSA criteria for moderate and severe infections and compared outcomes and complication

83 mic and transcriptomic changes characterized severe infections and death, and indicated impaired mito

84 model fungal pathogen and a common cause of severe infections and diseases.

85 Fewer severe infections and hospitalizations but more diarrhea

86 onic granulomatous disease, characterized by severe infections and inflammatory disorders.

87 splayed similar characteristics and rates of severe infections and inflammatory episodes that those o

88 H7N9 avian influenza virus causes severe infections and might have the potential to trigge

89 Severe infections and new-onset B-cell lymphoma occurred

90 fferentiate strains responsible for mild vs. severe infections and preference for hosts (e.g., animal

91 from siblings and was associated with fewer severe infections and pulmonary complications.

92 trophil disorders confer a predisposition to severe infections and reveal novel mechanisms that contr

93 ating crucial innate immune functions during severe infections and sepsis.

94 ren show a relative resistance to death from severe infections and sepsis.

95 hil extracellular traps(NETs) in response to severe infection, and CitH3 may be a potential biomarker

96 Hypoparathyroidism is associated with more severe infection, and immunoglobulin abnormalities are m

97 extracellular GGT activity resulted in more severe infections, and assay of immune response and tiss

98 ugh improved identification of children with severe infections, and better targeting of children in n

99 rine group and 11 in the rituximab group had severe infections, and cancer developed in 2 patients in

100 ed the incidence of all probable infections, severe infections, and hospitalization but did not inclu

101 sceptibility of HEU infants born in a HIC to severe infections, and that this effect could be related

102 However, knowledge is sparse regarding less severe infections, anti-infective treatment, and deliber

103 Severe infections are a major stress on haematopoiesis,

104 Less severe infections are more common and whether they are a

105 ied by STI or osteomyelitis and moderate and severe infections are not categorized separately.

106 ntibiotic resistance of pathogenic bacteria, severe infections are reported more frequently in medica

107 tious MCGN has a poor long-term outcome with severe infections as the main cause of death.

108 an acute febrile illness, 5-20% progress to severe infection associated with significant morbidity a

109 l kinase 2 (Tie2) are markedly imbalanced in severe infections associated with vascular leakage, yet

110 of natural T regulatory cells developed more severe infections, associated with elevated levels of IL

111 Patients have severe infections, autoimmunity, or both.

112 roviding facile access for bacteria to cause severe infection both in the pulp and systemically.

113 ent for young infants with signs of clinical severe infection but without signs of critical illness.

114 ent for young infants with signs of clinical severe infection but without signs of critical illness.

115 eficient NET formation predisposes humans to severe infection, but, paradoxically, dysregulated NET f

116 l combinations with therapeutic potential in severe infections, but there remains a need to substanti

117 In response to the emergence of severe infection capable of rapid global spread, WHO wil

118 n-meropenem combination for the treatment of severe infections caused by carbapenem-resistant, colist

119 n-meropenem combination for the treatment of severe infections caused by carbapenem-resistant, colist

120 last-resort antibiotic that is used to treat severe infections caused by extensively drug-resistant b

121 es, the associated endotoxin release (ER) in severe infections caused by gram-negative bacteria could

122 e control, noninferiority trials of selected severe infections caused by more susceptible pathogens.

123 Rickettsioses are severe infections caused by obligately intracellular bac

124 rimary immunodeficiencies that predispose to severe infections caused by severe acute respiratory syn

125 re primary immunodeficiency characterized by severe infections caused by weakly virulent mycobacteria

126 Streptococcus pneumoniae is responsible for severe infections, causing millions of deaths yearly.

127 sm; a similar cognitive decline also follows severe infection, chemotherapy, or trauma and is current

128 rophils in the lungs and other organs during severe infection contributes to sepsis-induced organ dys

129 osteomyelitis and evaluating if moderate and severe infection criteria improve the classification's a

130 Severe infections developed in 10 patients during emapal

131 Our study shows that in severe infections due to COS gram-negative bacteria, the

132 used as part of a last resort treatment for severe infections due to gram positive bacteria.

133 ndicate that neonates are more vulnerable to severe infections due to immaturity of their immune syst

134 ls of IL-27 predispose neonatal mice to more severe infection during Gram-negative sepsis.

135 atient antibiotic treatment for infants with severe infection during the neonatal period.

136 Along with recurrent and severe infections, especially cutaneous viral infections

137 m in immunocompromised hosts presenting with severe infections, especially if their history shows exp

138 arrier to effective triage and management of severe infections, especially in low-resource settings.

139 Enteroviruses can cause severe infections, especially in young children.

140 ts from ND subjects, and also, subjects with severe infection even presented a decrease in lipoprotei

141 Severe infections fell from 2.38 (95% CI 1.44-3.72) per

142 At present there is a focus on therapies for severe infections, for which effective treatment is most

143 not differ between groups, renal failure and severe infection-free survival were worse in those with

144 persistent neutropenia favours the spread of severe infections, frequently fungal infections.

145 No other severe infections, fungal or otherwise, were reported in

146 us) infections are among the most common and severe infections, garnering notoriety in an era of incr

147 the pathogenic role of contact activation in severe infections has not been well defined.

148 d this effect predominantly in patients with severe infections [hazard ratio, 1.41; 95% confidence in

149 In severe infections, hemostatic impairment is frequently o

150 is considered to be a prerequisite for these severe infections, however little is understood about th

151 sion (hazards ratio [HR], 1.83), episodes of severe infection (HR, 2.15), and estimated GFR (HR, 0.89

152 mortality (HR: 1.29; 95% CI: 1.03-1.61) and severe infections (HR: 2.79; 95% CI: 1.35-5.79).

153 group than in the supportive-care group had severe infections, impaired glucose tolerance, and weigh

154 Severe infections, impaired glucose tolerance, and/or we

155 causes brief moderate parasitization and no severe infection in chimpanzees.

156 Preterm infants are at significant risk of severe infection in early life and throughout childhood.

157 onatal mouse model of RSV infection to mimic severe infection in human infants.

158 ts associate Staphylococcus lugdunensis with severe infection in humans.

159 a leading cause of birth defects and causes severe infection in immunocompromised individuals.

160 , which have previously been associated with severe infection in immunologically naive hosts, are rar

161 main the first-choice empiric antibiotic for severe infection in many sub-Saharan African hospitals.

162 a Toro virus (PTV) has been shown to produce severe infection in mice, modeling disease caused by the

163 Herpes simplex virus (HSV) can cause severe infection in neonates leading to mortality and li

164 ococci as the most frequent pathogen causing severe infection in patients after splenectomy.

165 y in the elderly, the 2009 H1N1 virus caused severe infection in young adults.

166 or outpatient treatment of clinical signs of severe infection in young infants whose parents refused

167 9% of cases, including liver decompensation, severe infections in 10.4%, and death in 2.2%.

168 retion of ExoU has been associated with more severe infections in both humans and animal models.

169 To understand the impact of common severe infections in CGD, we examined the records of 268

170 ) is responsible for an escalating number of severe infections in children, but no prophylactics or t

171 Acinetobacter baumannii causes severe infections in compromised patients, who present a

172 nhibitors or ribavirin, in the management of severe infections in hospitalized patients and immunocom

173 d readily transmissible pathogens that cause severe infections in hospitalized patients. We discovere

174 ensal bacterium of dog's mouth flora causing severe infections in humans after dog bites or scratches

175 is an opportunistic pathogen that may cause severe infections in humans and other vertebrates.

176 to bind to human glycan receptors and cause severe infections in humans but have yet to adapt to and

177 Streptococcus (GAS) has been associated with severe infections in humans including necrotizing fascii

178 tentially with even greater ability to cause severe infections in humans or cause human-to-human tran

179 and the recently emerged H7N9 viruses cause severe infections in humans, often with fatal outcomes.

180 enza A viruses were responsible for numerous severe infections in humans, these viruses do not typica

181 ly pathogenic avian influenza A(H5N1) causes severe infections in humans.

182 tein hemagglutinin (HA) correlates with more-severe infections in humans.

183 " should be regarded as a potential cause of severe infections in humans.

184 r proteins and has been associated with more severe infections in humans.

185 opportunistic bacterial pathogens that cause severe infections in immunocompromised individuals and p

186 ged bacteremia in immunocompetent humans and severe infections in immunocompromised individuals.

187 sionally infect humans, causing particularly severe infections in immunocompromised individuals.

188 that has been occasionally reported to cause severe infections in immunocompromised patients.

189 may persist for months in young children and severe infections in immunosuppressed adults.

190 Human cytomegalovirus (HCMV) may cause severe infections in lung transplant recipients (LTRs).

191 ciated with preterm births, stillbirths, and severe infections in neonates and adults.

192 Aspergillus and Mucorales species cause severe infections in patients after hematopoietic stem c

193 nd varicella-zoster viruses (MMRV) may cause severe infections in seronegative adult solid organ tran

194 s oral lesions, encephalitis, keratitis, and severe infections in the immunocompromised host.

195 , primarily PeV-A3, as an important cause of severe infections in young children.

196 , primarily PeV-A3, as an important cause of severe infections in young children.

197 ther relevant pathogen-related biomarkers of severe infections include the involvement of specific cl

198 gistic regression analysis, risk factors for severe infection included pre-existing renal disease (od

199 the possible presentation of metastatic and severe infection, including osteomyelitis, due to the hy

200 Severe infection, including sepsis, is an increasing cli

201 he macrophage activation syndrome induced by severe infections, including in infections with the rela

202 ortunistic human pathogen capable of causing severe infections, including pneumonia and sepsis, in im

203 strate that pneumococcal pneumonia and other severe infections increase expression of multiple compon

204 ed mice with experimental COPD also had more severe infection (increased viral titer and pulmonary in

205 proportion of infected children who develop severe infection, increasing the children's susceptibili

206 ition could act to increase the incidence of severe infection: increasing the proportion of infected

207 Severe infections induce hyperinflammatory responses tha

208 ronically infected IL-25(-/-) mice developed severe infection-induced intestinal inflammation associa

209 causative microorganism(s) in patients with severe infection is crucial to optimize antimicrobial us

210 Possible severe infection is diagnosed in young infants (aged 0-5

211 The more severe infections lead to dengue hemorrhagic fever (DHF)

212 and immunological parameters to predict late severe infection (LI) beyond month 6 in solid organ tran

213 Occasionally, however, severe infection may arise, especially in very young chi

214 These severe infections may be prolonged or recurrent and add

215 ressive supportive care to determine whether severe infections might be avoided and hematologic outco

216 It has been previously hypothesized that severe infections might be due to reactivation of a pers

217 l antioxidant enzymes are overwhelmed during severe infections, mitochondrial dysfunction can occur a

218 t dysmotility or dysfunction (n=3), ACR with severe infection (n=1), and arterial graft aneurysm (n=1

219 Severe infections occur infrequently in pediatric patien

220 Late severe infection occurred in 104 patients (33.6%).

221 Grade 3 or 4 severe infections occurred in 7.7% of patients.

222 nfection with West Nile virus (WNV) causes a severe infection of the central nervous system (CNS) wit

223 West Nile virus (WNV) causes a severe infection of the central nervous system in severa

224 The virus causes tick-borne encephalitis, a severe infection of the CNS with a high risk for long-la

225 onocytogenes infection leads to abortion and severe infection of the fetus or newborn.

226 cytial virus is a human pathogen that causes severe infection of the respiratory tract.

227 eminate beyond the nasopharynx and to elicit severe infections of the middle ears, lungs, and blood t

228 Severe infections, often requiring ICU admission, have b

229 counterparts, the elderly do not respond to severe infection or injury with an exaggerated inflammat

230 ous immunoglobulin (IVIg) is widely used for severe infection or the treatment/prevention of antibody

231 une memory to influenza 1 year after mild or severe infection or vaccination.

232 ding to transplant before the development of severe infections or malignant transformation.

233 erns or due to increases in the frequency of severe infections or super-shedding events - population

234 an encouraging result given the potentially severe infection outcomes of this population.

235 .046), but it did not increase the number of severe infections (P = .812).

236 Predictors of a fatal outcome were severe infections, particularly in splenectomized cases,

237 wever, this regimen was also associated with severe infections, particularly when high doses of corti

238 The loss of Ifi44 was associated with a more severe infection phenotype in a mouse model of infection

239 These S. meliloti mutants induced a more severe infection phenotype on Mtlyk10 mutant plants.

240 e transfusions can be helpful in controlling severe infections progressing despite the use of appropr

241 GT resulted in a sustained reduction in the severe infection rate from 1.17 events per person-year t

242 Since treatments of severe infections remain effective up to three days post

243 Severe infections remain one of the main causes of neona

244 e independent risk factors for infection and severe infection requiring hospital admission.

245 ite this, patients clearly benefited in that severe infections resolved.

246 es to the relatively diminished frequency of severe infections seen with seasonal H3N2 influenza viru

247 Cure of severe infections, sepsis, and septic shock with antimic

248 umans and in mice, causing susceptibility to severe infections since early in life.

249 econdary to an underlying condition, such as severe infections, solid or hematologic malignancies, tr

250 onstrate that specific Th1 responses promote severe infection-stimulated alveolar bone loss.

251 titude of human diseases from pharyngitis to severe infections such as toxic shock syndrome and necro

252 at the expense of the host in conditions of severe infection, suggesting that MIF could represent a

253 We observed that severe infection symptoms are not necessarily correlated

254 cMSSA clones caused more severe infection than cMRSA clones.

255 a (IFNgamma), CXCL9, and CXCL10 and had more severe infection than EM patients carrying the 1805TG/TT

256 d, uninfected [HEU]) are more susceptible to severe infection than HIV-unexposed, uninfected (HUU) ch

257 found that such transgenic mice display more severe infection than wild-type littermates when treated

258 robial peptide cathelicidin experienced less severe infection than wild-type mice in a well-establish

259 Marburg virus causes a severe infection that is associated with high mortality

260 infections, particularly puerperal sepsis, a severe infection that occurs during or after childbirth.

261 erium Burkholderia pseudomallei, is an often severe infection that regularly involves respiratory dis

262 ngenital neutrophil deficiencies suffer from severe infections that are often fatal, underscoring the

263 ssociated (CA)-MRSA strains, which can cause severe infections that can result in necrotizing fasciit

264 Pseudomonas aeruginosa is a major cause of severe infections that lead to bacteremia and high patie

265 and reviews about cardiac complications and severe infections that result from long-term intravenous

266 roportion of infected children who developed severe infection, the population attributable fraction (

267 e spectrum that ranges from HLH secondary to severe infection to FHL.

268 ated a gene therapy trial for X-CGD to treat severe infections unresponsive to conventional therapy.

269 isms or with chronic, previously treated, or severe infections usually require broader spectrum regim

270 The respective rate of severe infection was 1.0 percent and 2.0 percent (P=0.15

271 o treat young infants with clinical signs of severe infection was as efficacious as an injectable pro

272 onella subspecies I serovars associated with severe infections, was confirmed to be located on the ch

273 innate immune responses are associated with severe infection, we measured the innate cells trafficki

274 Patients with severe infection were significantly more likely to have

275 dental splenectomy and risk of mortality and severe infections were analyzed using multivariable Cox

276 Cumulative incidences of severe infections were as follows: etanercept 48%, MMF 4

277 Severe infections were associated with earlier seroconve

278 Severe infections were seen in 21% of patients, and desp

279 t least 1 medication prescribed (i.e., more "severe" infections) were inversely associated with risk

280 significantly in frequency between mild and severe infection, which suggests protection against seve

281 eans of risk stratification of patients with severe infections, which suggests new avenues for therap

282 atified young infants with clinical signs of severe infection whose parents did not accept referral t

283 The lipid-enveloped Ebola virus causes severe infection with a high mortality rate and currentl

284 irectly and promoting immunopathology during severe infection with an intracellular bacterium.

285 Severe infection with EV71 can lead to neurological comp

286 Severe infection with EV71 can lead to various neurologi

287 Although lymphopenia is a hallmark of severe infection with highly pathogenic H5N1 and the new

288 nished antibody responses, resulting in more severe infection with increased SIV infectivity, a decre

289 We have previously shown that severe infection with Pseudomonas aeruginosa ultimately

290 en that replicates the signs and symptoms of severe infection with respiratory syncytial virus (RSV),

291 Melioidosis, a severe infection with the environmental bacterium Burkho

292 s periodic outbreaks in humans, resulting in severe infections with a high (60%) incidence of mortali

293 y deficiency (SPAD) revealed in adulthood by severe infections with encapsulated bacteria.

294 essive mutations characterised clinically by severe infections with mycobacteria.

295 une dysfunction that predisposes the host to severe infections with unrelated pathogens.

296 totoxic chemotherapy infrequently results in severe infections with viruses controlled by memory T ce

297 so more pronounced and longer lasting during severe infection, with concomitant changes in bile acids

298 asis in young infants with clinical signs of severe infection, without signs of critical illness, and

299 Determination of risk factors for severe infection would enable identifying patients who m

300 allograft dysfunction (CLAD) and graft loss, severe infection would.