ライフサイエンスコーパス: severe infection

1 sociated immune suppression in patients with severe infection.

2 icipants fulfilled prespecified criteria for severe infection.

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

4 drome involving complications as a result of severe infection.

5 ssociated with protection against common and severe infection.

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

7 wn about the mechanisms of susceptibility to severe infection.

8 fficient to provide benefit in management of severe infection.

9 compromised neutrophil recruitment, and more-severe infection.

10 g possible immuno-pathogenetic mechanisms of severe infection.

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

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

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

14 Coccidioidomycosis ranges from a mild to a severe infection.

15 thrombosis, and the major cause of death was severe infection.

16 rrelated with likelihood of acquiring a more severe infection.

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

18 ce treatment for young infants with clinical severe infection.

19 -threatening inflammatory response caused by severe infection.

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

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

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

23 mediated antiviral pathways and apoptosis in severe infection.

24 mmunity health worker with signs of clinical severe infection.

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

26 nd their release into circulation induced by severe infection.

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

28 ngers as potential adjuvant therapies during severe infections.

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

30 lize different virulence mechanisms to cause severe infections.

31 crobiota far more frequently than they cause severe infections.

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

33 e development and function and presents with severe infections.

34 e vital for controlling viral replication in severe infections.

35 n damage and improves animal survival during severe infections.

36 cated in contributing to the pathogenesis of severe infections.

37 ce factor for Staphylococcus aureus to cause severe infections.

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

39 cal devices are increasingly associated with severe infections.

40 lung diseases, Pandoraea species can produce severe infections.

41 nonmyeloablative and was not associated with severe infections.

42 kines that contribute to the pathogenesis of severe infections.

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

44 contaminated water can lead to outbreaks and severe infections.

45 ency that causes increased susceptibility to severe infections.

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

47 rade 4 hematologic toxicity and 6 documented severe infections.

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

49 Incidence of severe infection 10 years after transplantation was high

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

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

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

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

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

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

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

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

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

59 ection, graft pancreatitis, dehydration, and severe infections all decreased dramatically after the f

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

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

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

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

64 eas regions with poor perfusion are prone to severe infection and may require surgical debridement.

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

66 Severe infection and septic episodes increased in group

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

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

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

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

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

72 Fewer severe infections and hospitalizations but more diarrhea

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

74 Severe infections and neutropenia were more frequent wit

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

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

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

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

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

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

81 t goes wrong; underactivity resulting in the severe infections and tumours of immunodeficiency, overa

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

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

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

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

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

87 a with a variable effect on the incidence of severe infections, antibiotic usage, and the duration of

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

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

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

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

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

93 Patients have severe infections, autoimmunity, or both.

94 cus pyogenes infection, is less effective in severe infections because of its short postantibiotic ef

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

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

97 total cholesterol have been observed during severe infection, but it is not known whether the minor

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

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

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

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

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

103 Rickettsioses are severe infections caused by obligately intracellular bac

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

105 mice lacking a functional OPN gene had more severe infections characterized by heavier bacterial loa

106 treptococcus pyogenes and is associated with severe infections characterized by rash, hypotension, mu

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

108 cornea resulted in an earlier onset and more severe infection compared to controls.

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

110 observed among isolates from recent cases of severe infection does not support a clonal basis for the

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

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

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

114 n transplant recipients are also at risk for severe infections due to V vulnificus.

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

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

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

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

119 t in both groups), or decrease the number of severe infections (five in the G-CSF group vs. six in th

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

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

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

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

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

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

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

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

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

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

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

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

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

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

134 Staphylococcus aureus is a major cause of severe infection in humans and yet is carried without sy

135 ts associate Staphylococcus lugdunensis with severe infection in humans.

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

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

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

139 up B streptococci (GBS) are a major cause of severe infection in newborns, pregnant females, and othe

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

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

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

143 9% of cases, including liver decompensation, severe infections in 10.4%, and death in 2.2%.

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

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

146 Vibrio vulnificus is responsible for severe infections in chronically ill patients.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

161 ular, food-borne pathogen capable of causing severe infections in immunocompromised or pregnant indiv

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

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

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

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

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

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

168 Severe infection, including sepsis, is an increasing cli

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

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

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

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

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

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

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

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

177 spread use of ciprofloxacin in patients with severe infections is likely to result in alterations in

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

179 orms of SCID are characterized by recurrent, severe infections leading to death in infancy unless suc

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

181 These severe infections may be prolonged or recurrent and add

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

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

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

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

186 Severe infections occur infrequently in pediatric patien

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

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

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

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

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

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

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

194 Severe infections, often requiring ICU admission, have b

195 g injury occurs frequently in the setting of severe infection or blood loss.

196 for the "sickness behavior" of patients with severe infection or cancer, as well as for the neuropsyc

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

198 Severe infection or tissue invasion can provoke a catabo

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

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

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

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

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

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

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

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

207 Severe infections remain one of the main causes of neona

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

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

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

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

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

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

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

215 We observed that severe infection symptoms are not necessarily correlated

216 cMSSA clones caused more severe infection than cMRSA clones.

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

218 histology, in that strain SC5314 caused more severe infection than VE175 and the difference was stati

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

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

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

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

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

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

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

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

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

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

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

230 Children with severe, infection-triggered exacerbations of obsessive-c

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

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

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

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

235 Resistance to initial severe infection was associated with CD4+alpha beta+IFN-

236 ut hepatitis (11/15 vs. 10/39; P=0.002), but severe infection was not (9/15 vs. 15/39).

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

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

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

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

241 However, prolonged cytopenias and severe infections were more common in the higher 2CdA do

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

243 In addition, we reviewed 26 similar cases of severe infections which had previously been reported.

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

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

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

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

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

249 Severe infection with EV71 can lead to neurological comp

250 Severe infection with EV71 can lead to various neurologi

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

252 have been shown to confer susceptibility to severe infection with nontuberculous mycobacteria.

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

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

255 Melioidosis, a severe infection with the environmental bacterium Burkho

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

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

258 essive mutations characterised clinically by severe infections with mycobacteria.

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

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

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