ライフサイエンスコーパス: acute disease

1 ced IFN-gamma does not alter the severity of acute disease.

2 ) are required for the development of severe acute disease.

3 , by components of plasma from patients with acute disease.

4 , while infection with JHM.IA resulted in no acute disease.

5 ection, is not essential for inflammation in acute disease.

6 ntioxidant protection (R =.48; p =.00067) in acute disease.

7 in inducing specific CD8+ T cells during the acute disease.

8 r, but only a subset went on to develop more acute disease.

9 on recovered normally from passively induced acute disease.

10 eath (AICD) in the spontaneous recovery from acute disease.

11 d IL-10 (Ad-5/IL-10) reduced the severity of acute disease.

12 polysaccharide I (CPS I) to virulence during acute disease.

13 se, and the mice recovered more quickly from acute disease.

14 38), as previously reported in a cohort with acute disease.

15 3 billion just for those found to be free of acute disease.

16 with rapid, high-level viral replication and acute disease.

17 required for the in vitro properties or for acute disease.

18 oup and none in the combined group developed acute disease.

19 e analyzed to identify the major features of acute disease.

20 e encephalitis (JE) is a vaccine-preventable acute disease.

21 amsters, a species particularly sensitive to acute disease.

22 of long-term residency within the horse post-acute disease.

23 irectly related to signs and symptoms during acute disease.

24 -17A's ability to induce Th2 inflammation in acute disease.

25 y higher in the CNS at remission than during acute disease.

26 fever with renal syndrome (HFRS) is a severe acute disease.

27 pha, interleukin-10, and interferon-gamma in acute disease.

28 ere also reduced in Panx1 KO EAE mice during acute disease.

29 1 does not contribute to the pathogenesis of acute disease.

30 enal fibrosis in mouse models of chronic and acute disease.

31 al, unknown trigger is needed to bring about acute disease.

32 ng virus-host interactions in persistent and acute disease.

33 midine is also effective in a mouse model of acute disease.

34 ntly lower than those found in patients with acute disease.

35 nt the high-level bacteremia associated with acute disease.

36 plotype had reduced plasma MIF levels during acute disease.

37 s acquired or correlate with protection from acute disease.

38 on in children with malaria, but only during acute disease.

39 e functions that change during the course of acute disease.

40 t recipients receiving prophylaxis to reduce acute disease.

41 tic indicator or predicting other chronic or acute diseases.

42 uses may be implicated in chronic as well as acute diseases.

43 tions are linked to multiple degenerative or acute diseases.

44 r novel, host cell-focused therapies against acute diseases.

45 ilable in six patients and were decreased in acute disease (0.29 +/- 0.02 g/L) compared with convales

46 tive colitis during the study period: 73 for acute disease, 18 for advanced age and/or comorbidities,

47 f transferrin was significantly increased in acute disease (36.9% +/- 2.5%) compared with convalescen

48 issue activation in the head and neck during acute disease, a generalised pattern of peripheral lymph

49 gly, BIO 5192 treatment begun at the peak of acute disease accelerated entrance into disease remissio

50 ph (CXR) findings were classified as showing acute disease (AD; n=101) or no AD (NAD; n=92).

51 Designed to respond episodically to acute disease, almost all historical investment has focu

52 six types of EEHV in blood of elephants with acute disease, although EEHV1A is the predominant pathog

53 on of T(H)1-associated genes was detected in acute disease, although some were significantly upregula

54 iphasic disease, with T(H)2 predominating in acute disease and a switch to T(H)1 characterizing chron

55 CD4 and CD8(+) T cells were detected during acute disease and maintained to 12 years, but these decl

56 Understanding how ECM components aid acute disease and persistence could lead to improvements

57 le, as indicated by blocking and reversal of acute disease and reduced number of relapses and diminis

58 Prophylactic anti-IL-17A prevents acute disease and relapse and is associated with reduced

59 useful marker for leukemia in patients with acute disease and suggest a role for CREB in leukemogene

60 f drugs targeting short course therapies for acute diseases and towards long-term treatment of chroni

61 ticipate actively in the pathogenesis of the acute disease, and harbor the virus chronically, allowin

62 of T and B cell genes) persisted beyond the acute disease, and immune dysregulation was greatly impa

63 asma exchange, and pulse cyclophosphamide in acute disease, and strategies to prevent relapse over th

64 The adaA (acute disease antigen A) gene was detected in acute grou

65 Viral clearance and acute disease are associated with a strong, polyclonal,

66 oals infused with nonimmune plasma developed acute disease associated with high levels of the predomi

67 e brain during several neurodegenerative and acute diseases associated with infiltration of periphera

68 Ab's between 26 and 35 weeks of age reversed acute disease, blocked chronic disease, and extended the

69 Although the acute disease burden is sizeable, emerging data suggest

70 tomegalovirus (CMV) prophylaxis prevents the acute disease but its impact on subclinical infection an

71 IL-17A expression seems significant during acute disease but less important chronically.

72 n at this position (T81W) produced a similar acute disease but was attenuated for the development of

73 Many human viruses not only cause acute diseases but also establish persistent infections.

74 sets tolerized to MOG were protected against acute disease, but after tolerization treatment a lethal

75 e activated and initiate regeneration during acute disease, but lose this ability during the chronic

76 Four patients (9%) died during the acute disease, but most showed marked improvement with i

77 ate the clearance of infectious virus during acute disease by cell-mediated immunity.

78 The acute disease caused by ADV consists of permissive infec

79 may have direct application in prevention of acute disease caused by intracellular bacterial pathogen

80 -/- mice suffered an early and a more severe acute disease characterized by incomplete recovery when

81 High altitude and cold involve acute disease, chronic disease, and public health issues

82 plasmids that were originally isolated from acute-disease, chronic-disease, and severely attenuated

83 the treated group) and significantly reduced acute disease (clinical index of 4.3 +/- 0.7 in the untr

84 taken over a nine month period encompassing acute disease, convalescence, and recovery.

85 Prevention of acute disease could improve long-term lung health, with

86 tation (SBMT), when performed at the peak of acute disease (day 14), prevented glial scarring and ame

87 Acute disease developed with equal kinetics and severity

88 ither CD28 peptide mimic administered during acute disease dramatically improved clinical signs of EA

89 iral hepatitis in four U.S. counties who had acute disease during 1985 to 1986 or 1991 to 1995.

90 disease initiation or during remission from acute disease effectively blocks the expression of the i

91 Study I examined acute disease, either first presentation or relapse (Bir

92 ion in experimentally infected equids during acute disease episodes and during asymptomatic infection

93 ed by youth and a susceptibility to repeated acute disease episodes.

94 Acute disease exacerbations, due frequently to viral inf

95 ponders (group A, n=11) and untreated active/acute disease (group B, n=9) and compared to Caucasian h

96 Fifty-six percent of patients with acute disease had an improved maximal incisal opening af

97 In addition to acute disease, high altitude involves chronic mountain s

98 aemocanis is a blood pathogen that may cause acute disease in immunosuppressed or splenectomized dogs

99 redominant sites of virus replication during acute disease in infected equids and serve as resilient

100 sis is a highly infectious bacterium causing acute disease in mammalian hosts.

101 length or secreted gD2 significantly reduced acute disease in mice and guinea pigs (both P<.001) and

102 nged with group I isolates, mild to moderate acute disease in response to group V isolates, and no ac

103 ctivation in these cultures, and produced an acute disease in rhesus and pigtail macaques.

104 Development of acute disease in successfully vaccinated individuals is

105 ers S. equi significantly less able to cause acute disease in the natural host.

106 ev region from the avirulent parent, induced acute disease in two animals, while a similar infectious

107 cline, it is not known whether it relates to acute disease in younger healthy populations.

108 chronic diseases or can reactivate to cause acute diseases in AIDS patients or patients receiving im

109 cting contagion and the immediate outcome of acute diseases in previously healthy individuals is larg

110 Ducks developed acute disease, including severe neurological dysfunction

111 r cycle length and consisted of five states: acute disease, indeterminate disease, cardiomyopathy wit

112 e most advanced in development are targeting acute disease indications such as stroke, myocardial inf

113 During acute disease, infiltrating CD8(+) T cells secrete gamma

114 Acute disease is associated with C. jejuni invasion of t

115 The acute disease is characterized by systemic mycobacterial

116 ce of optimal chemotherapeutic intervention, acute disease is frequently fatal.

117 In the absence of IL-2, the acute disease is mild because of reduced T cell effector

118 Acute disease of the upper respiratory tract usually inv

119 the simplest cases: short-term prediction in acute diseases of otherwise healthy persons.

120 sease phase but increase significantly after acute disease onset on cardiomyocyte death and fibrotic

121 154 antibody treatment at either the peak of acute disease or during remission effectively blocked cl

122 contrast, Ab treatment either at the peak of acute disease or during remission exacerbated disease re

123 blood cells were isolated during the initial acute disease or from asymptomatic animals and analyzed

124 al hearing loss (SNHL) in the late stages of acute disease or in early convalescence.

125 r VB families revealed their presence during acute disease or relapses but, with the exception of VB1

126 ere depleted immediately before the onset of acute disease, or during the chronic stage, a striking a

127 d to P. vivax infection; in the remaining 4, acute diseases other than malaria were found to be the c

128 ease who do not meet the case definition for acute disease pose a low infection risk to health-care p

129 and IL-10(-)CD8 T cells interconvert during acute disease, possibly based on recent Ag exposure.

130 V-specific T-cell responses generated during acute disease predominantly target ORF2, but decline in

131 osts, and this is often associated with more acute disease presentation.

132 CRP treatment of NZB/NZW mice during acute disease rapidly decreased proteinuria, and the tre

133 In the cuprizone model, acute disease reduces serum cholesterol levels that can

134 ranscriptional and cytokine responses during acute disease reflected dominant type I/II interferon si

135 n contrast, uPAR-/- mice had a delayed, less acute disease reflected in delayed infiltration of infla

136 r endogenous myelin epitopes released during acute disease, reflecting a critical role for epitope sp

137 ral IL-17A mRNA expression quantified during acute disease, remission, and relapse.

138 However, the acute disease resolved, and the CB6F(1) mice went on to

139 Hantavirus pulmonary syndrome (HPS) is an acute disease resulting from infection with any one of a

140 f convergent evolution in isolates from post-acute disease samples as a result of niche adaptation to

141 Horses with acute disease served as a basis for comparison.

142 x (MHC) class I, and perforin contributed to acute disease signs at 8 days postinfection (p.i.).

143 ients with anti-NMDAR encephalitis after the acute disease stage and 25 healthy control subjects unde

144 ui within the horse is defined by short-term acute disease, strangles, followed by long-term infectio

145 Aggressive approaches to acute diseases such as acute myocardial infarction, trau

146 tem for mLcn2 in studies of animal models of acute diseases such as kidney and cardiac failure.

147 The introduction of vaccination against acute diseases such as measles induced a dramatic declin

148 Chronic diseases have overtaken acute diseases, such as infections, as the major cause o

149 arameters and in a guinea pig fever model of acute disease, suggesting a difference in virulence pote

150 nsory, neurons.IMPORTANCE Stress exacerbates acute disease symptoms resulting from HSV-1 and HSV-2 in

151 ble axonal dysfunction, which coincides with acute disease symptoms.

152 in-2(-/-)mice leads to a rapid appearance of acute disease symptoms.

153 xtensive lymphocyte activation and induce an acute disease syndrome in macaque monkeys.

154 ral mononuclear cell cultures and induces an acute disease syndrome in macaque monkeys.

155 Our data indicate that the acute disease syndrome induced by SIVmac239/YEnef is not

156 ntration of Legionella pneumophila causes an acute disease that is resolved by innate immune response

157 Arboviruses cause acute diseases that increasingly affect global health.

158 features, including the rapid development of acute disease, the episodic nature of chronic disease, t

159 During acute disease, the predominant cellular site of viral in

160 iruses affect host physiology beyond causing acute disease, thereby giving rise to the concept that t

161 Acute disease was also associated with significant incre

162 A, USA) in Malawian NTS cases (n=106) during acute disease was correlated with genotype by linear reg

163 genic events are required for progression to acute disease, we crossed hMRP8p210BCR/ABL mice to apopt

164 like the T-cell infiltrates that peak during acute disease, we found that microglia activation persis

165 Isolates associated with acute disease were found to be distinct from a group of

166 those isolated from naive mice or mice with acute disease, were able to endogenously present a varie

167 Guinea pigs developed severe acute disease when aerosol challenged with group I isola

168 ease in response to group V isolates, and no acute disease when infected with group IV and VI isolate

169 ein-reactive cells infiltrate the CNS during acute disease, whereas affinities during remission, rela

170 ely related to known genotypes from cases of acute disease, whereas the seven loci (4.0 kb) obtained

171 and CCL5, were prominently expressed during acute disease, whereas transcripts for CXCL9, CXCL10, an

172 high level of HIV gene expression developed acute disease which resulted in premature death, and mic

173 UL19/UL47 adenovirus groups developed severe acute disease, while 2/8 animals in the gC2/gD2-only gro

174 play an important role in protection against acute disease, while both CD4 T cells and antibodies are

175 la pertussis is the etiological agent of the acute disease whooping cough in infants and young childr

176 Both of these cause acute disease (whooping cough), whereas their progenitor

177 n that causes source-originated epidemics of acute disease with a case fatality rate thought to vary

178 s (DENV) that ranges from febrile illness to acute disease with serious complications.

179 detectable infection of challenge virus and acute disease within several weeks.

180 20%) was characterized by a more aggressive acute disease within the 48 hours preceding ICU admissio