ライフサイエンスコーパス: acute hepatitis

1 virus (HEV) is a human pathogen that causes acute hepatitis.

2 tective effects of BV in models of shock and acute hepatitis.

3 her asymptomatic or present with symptomatic acute hepatitis.

4 g telithromycin, the patients presented with acute hepatitis.

5 ent in the mouse liver within the context of acute hepatitis.

6 that clinically and pathologically resembles acute hepatitis.

7 wild-type-like acute infection and developed acute hepatitis.

8 s C virus (HCV), infects tamarins and causes acute hepatitis.

9 s of laboratory tests were characteristic of acute hepatitis.

10 sappeared concordant with the development of acute hepatitis.

11 cificity to patients who have recovered from acute hepatitis.

12 ms underlying the expression of IL-33 during acute hepatitis.

13 les of these processes in the development of acute hepatitis.

14 more abundant and sustained in children with acute hepatitis.

15 through the Sentinel County Surveillance for Acute Hepatitis (1998 to 2006).

16 most common type of toxic liver disease was acute hepatitis (33.5 %).

17 ) accounts for approximately 20% of cases of acute hepatitis, 70% of chronic hepatitis, and 30% of en

18 serum samples from patients with acute Hepatitis A (12/ 75 in Tel-Aviv and 31 patients ho

19 The incidence of acute hepatitis A and B infection has declined significa

20 Given the public health implications of acute hepatitis A and hepatitis B in patients with CLD,

21 because a large proportion of patients with acute hepatitis A do not have any identifiable risk fact

22 Acute hepatitis A is a major public health problem in de

23 Acute hepatitis A superimposed on chronic liver disease

24 culture or present in sera from humans with acute hepatitis A.

25 gnificant impact on the overall incidence of acute hepatitis A.

26 In a murine model of acute hepatitis, administration of a PD-1H agonist mAb s

27 The virus caused acute hepatitis after intravenous inoculation into Afric

28 on was investigated as the possible cause of acute hepatitis among 88 military patients stationed at

29 cytokine family, positively correlates with acute hepatitis and chronic liver failure in mice and hu

30 ratios for P falciparum malaria and also for acute hepatitis and HIV/AIDS.

31 the liver is critical for viral clearance in acute hepatitis and in the pathogenesis of chronic infla

32 1d-dependent, nonclassical NKT cell-mediated acute hepatitis and liver injury.

33 tion is usually self-limited but may lead to acute hepatitis and rarely to fulminant hepatic failure.

34 requently fails to occur after recovery from acute hepatitis and that traces of virus can maintain th

35 atitis E virus (HEV) is a causative agent of acute hepatitis, and it is the sole member of the genus

36 tion prolongs survival times of patient with acute hepatitis associated with alcoholic liver disease

37 ths after OLT) and the other patient died of acute hepatitis B (7 months after OLT).

38 ded us to identify the changing incidence of acute hepatitis B (AHB) in children and young adults.

39 t patients infected during adulthood develop acute hepatitis B (AHB), which usually results in viral

40 ly 1992, a 47-year-old woman became ill with acute hepatitis B after undergoing a thymectomy in which

41 from 134 individuals including patients with acute hepatitis B and C as well as chronic hepatitis B,

42 Reported cases of symptomatic acute hepatitis B and hepatitis C occurring in persons>/

43 t in two (11%) of 19 Caucasian patients with acute hepatitis B and nine (27%) of 33 Caucasian patient

44 ibe the results of enhanced surveillance for acute hepatitis B at 7 federally funded sites over a 6-y

45 using whole-genome sequences (n = 179) from acute hepatitis B cases (n = 1,206) identified through t

46 lness, suggesting that more than half of the acute hepatitis B cases might have been prevented throug

47 In the 6-year period, 2220 acute hepatitis B cases were reported from the 7 sites.

48 to factors potentiating hepatic damage with acute hepatitis B contributed to the outbreak's high mor

49 uring this period, the reported incidence of acute hepatitis B declined by 76.1% from 13.8 cases per

50 analysis of HBV whole genomes from cases of acute hepatitis B identified from 1998 to 2006 in the Un

51 irectly proportional to tissue injury during acute hepatitis B in humans.

52 n encouraging trend is that the incidence of acute hepatitis B in the United States declined as much

53 riod of decline in the reported incidence of acute hepatitis B in the United States.

54 ca. 2002, coinciding with transient rises in acute hepatitis B notification rates among adults; D3 un

55 Death related to acute hepatitis B occurs in approximately 1% of patients

56 hich a thoracic-surgery resident who had had acute hepatitis B six months earlier assisted.

57 increased level of arginase in patients with acute hepatitis B suppresses the functions of activated

58 f T-bet in virus-specific CD8 T cells during acute hepatitis B virus (HBV) and hepatitis C virus (HCV

59 Some patients with acute hepatitis B virus (HBV) infection develop chronic

60 Clearance of acute hepatitis B virus (HBV) infection is associated wi

61 Recovery from acute hepatitis B virus (HBV) infection occurs in 95% of

62 Recovery from acute hepatitis B virus (HBV) infection requires a broad

63 During acute hepatitis B virus (HBV) infection viral loads reac

64 Following an acute hepatitis B virus (HBV) infection, clearance or pe

65 ogical profile suggesting a previous cleared acute hepatitis B virus (HBV) infection, including high

66 Acute hepatitis B virus (HBV) infections either resolve

67 cratic drug-induced liver injury DILI (22%), acute hepatitis B virus infection (12%), autoimmune hepa

68 iral antigens in a transgenic mouse model of acute hepatitis B virus infection.

69 982-1998, enhanced sentinel surveillance for acute hepatitis B was conducted in 4 counties in the Uni

70 A total of 362 of 11 311 (3.2%) cases with acute hepatitis B were vaccinated.

71 lood mononuclear cells from 67 patients with acute hepatitis B, and 12 patients convalescent from acu

72 In liver biopsy specimens from patients with acute hepatitis B, but not chronic hepatitis B or contro

73 nvasive Haemophilus influenzae type b (Hib), acute hepatitis B, hepatitis A, varicella, Streptococcus

74 s targeted since 1980 including hepatitis A, acute hepatitis B, Hib, and varicella.

75 ompensated cirrhosis, organ transplantation, acute hepatitis B, pregnancy, coinfection with hepatitis

76 In patients with acute hepatitis B, the expansion of activated and prolif

77 ully vaccinated individuals among cases with acute hepatitis B, the proportion of preventable cases i

78 patitis B, and 12 patients convalescent from acute hepatitis B, were stimulated with three panels of

79 plays a central role in the pathogenesis of acute hepatitis B.

80 medicine clinic in the UK was diagnosed with acute hepatitis B.

81 s) using blood samples from 18 patients with acute hepatitis B.

82 quence changes were easily detectable in the acute, hepatitis B e antigen-positive phase of infection

83 atitis A virus (HAV), the causative agent of acute hepatitis, barely grows in cell culture and in the

84 te that JUNB/AP-1 promotes cell death during acute hepatitis by regulating IFN-gamma production in NK

85 We identified 20 participants with acute hepatitis C (10 with hepatitis C virus [HCV] monoi

86 to develop chronic hepatitis than those with acute hepatitis C (23% vs. 68%; P < .05).

87 Therapy of acute hepatitis C (AHC) has not yet been standardized an

88 Treatment of patients with acute hepatitis C (AHC) is more effective, with sustaine

89 ortion of HIV(+) patients manage to overcome acute hepatitis C (AHC) spontaneously.

90 ease resolution in a cohort of patients with acute hepatitis C (AHC), analyzing epidemiological, clin

91 els of IP-10, with outcomes of patients with acute hepatitis C (AHC).

92 The Australian Trial in Acute Hepatitis C (ATAHC) was a prospective study of the

93 ubjects, enrolled in the Australian Trial in Acute Hepatitis C (ATAHC), using HCV peptide enzyme-link

94 Approximately three quarters of acute hepatitis C (HCV) infections evolve to a chronic s

95 We examined trends in incidence of acute hepatitis C among young persons reported to the Ce

96 e epidemiologically distinct from those with acute hepatitis C and have a significantly more severe a

97 are essential for spontaneous resolution of acute hepatitis C and long-term protection from persiste

98 emed essential for spontaneous resolution of acute hepatitis C and long-term protection.

99 Patients with acute hepatitis C and schistosomiasis coinfection cannot

100 Acute hepatitis C and spontaneous clearance was also ass

101 Acute hepatitis C and spontaneous clearance was associat

102 ants identified from the Australian Trial in Acute Hepatitis C and the Networks study were followed l

103 cal correlates of clearance in patients with acute hepatitis C and their sexual contacts.

104 Further, PBMC from patients with acute hepatitis C as well as HCV-infected Huh7.5 cells h

105 markedly prolonged the incubation period of acute hepatitis C but did not prevent or delay HCV infec

106 covery occurs in a minority of patients with acute hepatitis C but is associated with vigorous and lo

107 Clinically, acute hepatitis C can increase concentrations of alanine

108 ceptor (TLR) expression and signaling during acute hepatitis C correlates with clinical outcomes.

109 Approximately 85% of persons with acute hepatitis C develop chronic hepatitis as determine

110 nclude that approximately 85% of people with acute hepatitis C develop persistent viremia.

111 Acute hepatitis C developed in both the IGIV-treated and

112 ells from healthy controls and patients with acute hepatitis C efficiently recognized both HCV-infect

113 Although the incidence of acute hepatitis C has declined, there is a large reservo

114 virin and also with spontaneous clearance of acute hepatitis C in a heterogeneous population.

115 d the efficacy of PEG IFN-alpha treatment in acute hepatitis C in relation to the kinetics of hepatit

116 mately 10% of persons with reported cases of acute hepatitis C in the United States report a history

117 Reports of acute hepatitis C in young persons in the United States

118 From 2006 to 2012, reported incidence of acute hepatitis C increased significantly in young perso

119 Peginterferon alfa-2b monotherapy in acute hepatitis C induces high sustained virologic respo

120 s with FPAs were compared with patients with acute hepatitis C infection without FPAs.

121 In acute hepatitis C infection, close monitoring of hepatit

122 There is a paucity of information on core in acute hepatitis C infection.

123 od samples from participants in the Montreal Acute Hepatitis C Injection Drug User Cohort Study who w

124 Our results show that the outcome of acute hepatitis C is associated with a functional hierar

125 The outcome of acute hepatitis C is associated with efficient virus-spe

126 Acute hepatitis C is marked by appearance of HCV RNA in

127 Acute hepatitis C is most often diagnosed in the setting

128 chronic hepatitis C, but neither its role in acute hepatitis C nor the biologic basis for its action

129 Mechanisms by which spontaneous clearance of acute hepatitis C occurs are unclear.

130 Symptomatic acute hepatitis C occurs in only about 15% of patients w

131 A patient developed acute hepatitis C shortly after tissue transplantation.

132 ve used this resource to study parameters of acute hepatitis C virus (HCV) infection among 94 donor-r

133 r (NK) cells likely contribute to outcome of acute hepatitis C virus (HCV) infection and interferon (

134 e a patient with hypogammaglobulinemia whose acute hepatitis C virus (HCV) infection appeared to reso

135 Outbreaks of acute hepatitis C virus (HCV) infection are occurring in

136 Acute hepatitis C virus (HCV) infection becomes chronic

137 Acute hepatitis C virus (HCV) infection culminates in vi

138 Although 20%-40% of persons with acute hepatitis C virus (HCV) infection demonstrate spon

139 sequelae during the first two decades after acute hepatitis C virus (HCV) infection have been well s

140 tween IL28B and the clinical presentation of acute hepatitis C virus (HCV) infection in a homogeneous

141 Fibrosis progression after acute hepatitis C virus (HCV) infection in human immunod

142 ness and cost-effectiveness of screening for acute hepatitis C virus (HCV) infection in human immunod

143 Acute hepatitis C virus (HCV) infection is often asympto

144 Acute hepatitis C virus (HCV) infection is rarely studie

145 Acute hepatitis C virus (HCV) infection is underdiagnose

146 Treatment of acute hepatitis C virus (HCV) infection leads to a susta

147 une responses during the first few months of acute hepatitis C virus (HCV) infection seem crucial for

148 guidelines now recommend that patients with acute hepatitis C virus (HCV) infection should be treate

149 Acute hepatitis C virus (HCV) infection was the final di

150 Historically, acute hepatitis C virus (HCV) infection was treated with

151 over, these cells were highly permissive for acute hepatitis C virus (HCV) infection, and persistent

152 e thought to be important for the control of acute hepatitis C virus (HCV) infection, but to date lit

153 In acute hepatitis C virus (HCV) infection, programmed deat

154 In the setting of acute hepatitis C virus (HCV) infection, robust HCV-spec

155 In studies of acute hepatitis C virus (HCV) infection, the early host

156 c liver disease may develop many years after acute hepatitis C virus (HCV) infection, the past incide

157 e early events that determine the outcome of acute hepatitis C virus (HCV) infection, we compared the

158 are the hallmark of spontaneous clearance of acute hepatitis C virus (HCV) infection, whereas compara

159 therapy has not been adequately evaluated in acute hepatitis C virus (HCV) infection.

160 ics and evolution predict outcome of primary acute hepatitis C virus (HCV) infection.

161 variation is a determinant of recovery from acute hepatitis C virus (HCV) infection; however, to dat

162 estigation was to prospectively characterize acute hepatitis C virus (HCV) infections and to evaluate

163 States, the annual number of newly acquired acute hepatitis C virus (HCV) infections has declined fr

164 Acute hepatitis C virus (HCV) is typically defined as ne

165 ered for 8, 12, or 24 weeks in patients with acute hepatitis C virus infection a total of 161 patient

166 Spontaneous resolution of acute hepatitis C virus infection cannot be predicted, a

167 These findings indicate that, during acute hepatitis C virus infection in vivo, virus-specifi

168 ed virologic response rates in patients with acute hepatitis C virus infection, thus preventing devel

169 a total of 161 patients were identified with acute hepatitis C virus infection.

170 ks in addition to 14 untreated subjects with acute hepatitis C were prospectively followed.

171 and immunological studies on 7 patients with acute hepatitis C who received antiviral therapy and wer

172 Forty subjects with proven acute hepatitis C who received either PEG IFN-alpha plus

173 Of 45 patients with acute hepatitis C, 40.0% were simultaneously infected wi

174 Compared with patients with acute hepatitis C, those with non-ABCDE hepatitis had a

175 ther these observations indicate that during acute hepatitis C, virus evolution was driven primarily

176 egylated interferon alfa-2b for treatment of acute hepatitis C.

177 longitudinally from the time of diagnosis of acute hepatitis C.

178 as playing a critical role in the outcome of acute hepatitis C.

179 drome of chronic liver GVHD presenting as an acute hepatitis can be recognized in a patient at risk w

180 HCV infection can result in acute hepatitis, chronic hepatitis, and cirrhosis, which

181 3 had preexisting HCV and the cause of their acute hepatitis could not be determined; of the remainin

182 levels of arginase observed in patients with acute hepatitis could suppress the function of activated

183 on, during acute flares of disease, and with acute hepatitis D superinfection.

184 , the patient developed an unexpected severe acute hepatitis despite persistence of anti-HBs.

185 for many years after clinical recovery from acute hepatitis, despite the presence of serum antibodie

186 The delayed onset of acute hepatitis does not result from delayed recruitment

187 nfected children with or without evidence of acute hepatitis during the first year of life.

188 In total, 2713 acute hepatitis E cases were diagnosed, of which 1376 we

189 A case of acute hepatitis E in a researcher following a scalpel in

190 were assembled from blood donors (n = 372), acute hepatitis E patients (n = 94), five laboratory ani

191 Several cases of acute hepatitis E showed portal and periportal hepatitis

192 Acute hepatitis E virus (HEV) infection is a leading cau

193 eripheral blood and liver tissue revealed an acute hepatitis E virus infection (genotype 3).

194 the past decade, an increasing frequency of acute hepatitis E was noted in Germany and other Europea

195 9 patients with anti-HEV IgM indicated that acute hepatitis E was the most likely diagnosis for 7 an

196 les, typhoid and parathyroid, leishmaniasis, acute hepatitis E, and HIV/AIDS), we used natural histor

197 man sera obtained 2 months to 13 years after acute hepatitis E, and postinoculation chimpanzee sera),

198 ely) in normal rats and in rats with induced acute hepatitis, fatty liver, or cirrhosis.

199 during immunosuppression can lead to severe acute hepatitis, fulminant liver failure, and death.

200 Recurring outbreaks of acute hepatitis have been a significant cause of morbidi

201 oups with hepatitis C, such as patients with acute hepatitis, human immunodeficiency virus coinfectio

202 w for the first time in an animal model that acute hepatitis impairs the repair of oxidative DNA base

203 th chimpanzees and rhesus monkeys and caused acute hepatitis in both.

204 We induced acute hepatitis in C57BL/6 mice by intravenous injection

205 virus (HEV) infections are a major cause of acute hepatitis in developing and industrialized countri

206 (HEV) is an emerging virus causing epidemic acute hepatitis in developing countries as well as spora

207 Theiler's disease is an acute hepatitis in horses that is associated with the ad

208 Hepatitis E virus (HEV) induces acute hepatitis in humans with a high fatality rate in p

209 navirus, mouse hepatitis virus (MHV), causes acute hepatitis in its natural host and provides a usefu

210 s been found to prevent injury in a model of acute hepatitis in mice through downregulation of tumor

211 y to wild-type virus but was unable to cause acute hepatitis in mice.

212 elated to hepatitis C virus (HCV) and causes acute hepatitis in tamarins (Saguinus species), making i

213 GB virus-B (GBV-B) causes an acute hepatitis in tamarins characterized by increased a

214 IL-33 in hepatocytes is blocked during ConA-acute hepatitis in TRAIL-deficient mice compared to WT m

215 Induction of acute hepatitis in wild-type C57BL/6 mice released large

216 was investigated after the induction of ConA-acute hepatitis in wildtype (WT), perforin(-/-) , tumor

217 ccine capable of protecting chimpanzees from acute hepatitis induced by challenge with heterologous v

218 In conclusion, PEG IFN-alpha therapy in acute hepatitis induces high rates of sustained virologi

219 d mortality using natural history models for acute hepatitis infections and GBD's cause-of-death ense

220 at eventually became chronic carriers had an acute hepatitis involving the same cell types, but at di

221 arance of the hepatitis B virus (HBV) during acute hepatitis is associated with a strong, polyclonal,

222 The expression of IL-33 during acute hepatitis is dependent on TRAIL, but not on FasL o

223 ther products, in contrast, tend to cause an acute hepatitis-like injury.

224 < .01) but were significantly reduced in the acute hepatitis model (82% and -36%, respectively).

225 ), new anti-HCV seropositivity with clinical acute hepatitis (n=21), or HCV strain sequencing after a

226 [n = 6]) and diffuse liver diseases (induced acute hepatitis [n = 6], fatty liver [n = 6], or cirrhos

227 ermine the disease etiology in patients with acute hepatitis of unknown etiology (HUE), serum specime

228 Every specificity shown during acute hepatitis persisted in normal liver tissue more th

229 The events were acute hepatitis, respiratory failure, pneumonia, atrial

230 is of liver-infiltrating immune cells during acute hepatitis revealed that expression of P2Y(2)R in b

231 ella abortus 2308 at 5 x 10(5) CFU developed acute hepatitis similar to many natural hosts but, unlik

232 or not with hemophagocytic syndromes, and to acute hepatitis syndromes.

233 r, CH1581 and CH1579 developed a less severe acute hepatitis than CH1422.

234 subjects, viremia was higher at the peak of acute hepatitis than it was when the disease began, and

235 the virus experienced a prolonged episode of acute hepatitis that coincided with a CD38+ IFN-gamma- C

236 e to hepatitis B virus and in the subsequent acute hepatitis that ensues.

237 health care workers, four of whom developed acute hepatitis that progressed to chronicity while one

238 titers of >10(4.7) IU/mL, and development of acute hepatitis; the chronicity rate was 56%.

239 Acute hepatitis then occurred after the withdrawal, or d

240 binant virus to infect tamarins and to cause acute hepatitis was determined.

241 Acute hepatitis was induced in C56BL/6N mice by administ

242 Using an in vivo Con A challenge model of acute hepatitis, we observed reduced survival and increa

243 d survived an average of 10 days, dying from acute hepatitis with an extensive hepatic infiltration o

244 morrhagic shock syndrome and less frequently acute hepatitis with liver failure and encephalopathy.

245 Hepatitis E virus infection causes an acute hepatitis with spontaneous resolution in the major

246 d animals by tail vein injection resulted in acute hepatitis, with a variety of pathological findings

247 E virus (HEV) infection is a major cause of acute hepatitis worldwide.