ライフサイエンスコーパス: FHF

1 FHF binding to IB2 facilitates recruitment of the MAPK p

2 FHF can be modeled in mice by administration of azoxymet

3 FHF has been reported in three families-the original Iri

4 FHF is a formidable clinical problem associated with a h

5 FHF is usually accompanied by massive hepatocellular dea

6 FHF rat livers exhibited reduced amino acid uptake, a sw

7 FHF-induced recruitment of p38delta to IB2 is accompanie

8 FHF/IB2 interaction is highly specific, as FHFs do not b

9 n pressure (CPP) before and during OLT in 12 FHF patients undergoing transplantation.

10 complex (t-Bu-bpy)Pd(IV)(p-FC(6)H(4))(F)(2)(FHF) (t-Bu-bpy = 4,4'-di-tert-butyl-2,2'-bipyridine).

11 Additionally, 42 FHF rats were killed in batches of six rats each 2, 6, 1

12 Two of 50 FHF (4%) and 10 of 104 control patients (10%) had EBV DN

13 Three of 50 FHF (6%) and 14 of 104 control patients (13%) were posit

14 ould be considered more frequently for adult FHF patients.

15 All FHF rats became comatose by 24 hours postoperatively.

16 imary cardiac Nav channel Nav1.5) that alter FHF binding result in human cardiovascular disease.

17 V DNA was observed in 3 of 10 North American FHF patients (30%) and 3 of 59 controls (5%) without ser

18 multipoint linkage analyses indicate that an FHF gene is likely to be located in an 8-cM interval bet

19 can rescue both ventricular SHF addition and FHF integrity.

20 rain is serine/threonine-phosphorylated, and FHF can serve as a substrate for p38delta in vitro.

21 , which compromises both SHF recruitment and FHF ventricular integrity.

22 hydrogen bond strength in bifluoride anion (FHF-).

23 case a bifluoride complex Tp'Rh(PMe3)(C5NF4)(FHF) was crystallized.

24 In transiently transfected 293 cells FHF-1 accumulates in the nucleus and is not secreted.

25 The majority of cryptogenic FHF cases cannot be attributed to infection with herpes

26 The mutations also disabled FHF modulation of voltage-dependent fast inactivation of

27 han hepatocytes in fVIII biosynthesis during FHF.

28 l be useful in characterizing changes during FHF, and in elucidating the effects of nutritional suppl

29 Each FHF is expressed in the developing and adult nervous sys

30 d 71% amino acid sequence identity, but each FHF shows less than 30% identity when compared with othe

31 fibroblast growth factor homologous factor (FHF) proteins to delay Nav inactivation, distal axonal N

32 HF2B, a member of the FGF homologous factor (FHF) subfamily, as an interacting partner of Na(v)1.6.

33 n-A, non-B, non-C fulminant hepatic failure (FHF) (3 patients), graft-versus-host disease (4 patients

34 During human fulminant hepatic failure (FHF) circulating levels of most hemostatic proteins fall

35 for patients with fulminant hepatic failure (FHF) continues to be unmet.

36 Patients with fulminant hepatic failure (FHF) die with brain edema, exhibiting an increased cereb

37 ale who developed fulminant hepatic failure (FHF) during the second trimester of pregnancy and underw

38 Fulminant hepatic failure (FHF) in humans produces a bleeding diathesis due in larg

39 r mass, otherwise fulminant hepatic failure (FHF) may arise.

40 Patients with fulminant hepatic failure (FHF) often die awaiting liver transplantation.

41 on patients with fulminant hepatic failure (FHF) or chronic liver disease (cirrhosis) was investigat

42 l animal model of fulminant hepatic failure (FHF) resembling the clinical condition is needed.

43 d transplants for fulminant hepatic failure (FHF) were stratified separately from those having an ele

44 hways affected by fulminant hepatic failure (FHF) would help develop nutritional support and other no

45 ive treatment for fulminant hepatic failure (FHF), but its use is limited because of organ donor shor

46 ive treatment for fulminant hepatic failure (FHF), but postOLT mortality is higher for patients with

47 n-A, non-B (NANB) fulminant hepatic failure (FHF), but the frequency of infection with these agents h

48 ere patients with fulminant hepatic failure (FHF), in group 2 (n = 3) were patients with primary nonf

49 ntation (OLT) for fulminant hepatic failure (FHF), some patients develop cerebral injury secondary to

50 tresia (EHBA) and fulminant hepatic failure (FHF).

51 TV in cryptogenic fulminant hepatic failure (FHF).

52 in patients with fulminant hepatic failure (FHF).

53 all children with fulminant hepatic failure (FHF).

54 but rarely cause fulminant hepatic failure (FHF).

55 unknown, and only familial Hibernian fever (FHF) has been described as a distinct clinical entity.

56 erized of which is familial Hibernian fever (FHF).

57 in the previously discovered FTS/Hook/FHIP (FHF) complex, which contains, besides FHIP and Hook prot

58 ook-FTS and Hook-interacting protein (FHIP) (FHF) complex, which interacts with the minus-end-directe

59 stinct sets of first and second heart field (FHF and SHF, respectively) progenitors.

60 ardium) develops from the first heart field (FHF) and expands by adding second heart field (SHF) cell

61 ardiac progenitors of the first heart field (FHF) do not require TBX1 and segregate precociously from

62 rdiomyocytes derived from first heart field (FHF) progenitors assemble the linear heart tube.

63 s), and second, a loss of first heart field (FHF) ventricular cardiomyocytes due to disrupted cell po

64 populations, first and second heart fields (FHF, SHF), sequentially contribute to longitudinal subdi

65 liver transplant (OLT) and chemotherapy for FHF secondary to PHL.

66 rates that LT is the treatment of choice for FHF and results in durable survival.

67 undertaken of all patients undergoing LT for FHF at a single transplant center.

68 Between 1984 and 2008, all LT for FHF performed in recipients less than or equal to 18 yea

69 ne of the largest published series on LT for FHF, demonstrates a long-term survival of nearly 70% and

70 examine predictors of survival after LT for FHF.

71 edian age 20.2 years) required urgent LT for FHF.

72 e 3 patients developing AA following OLT for FHF achieved hematologic recovery 21 and 92 days after d

73 The 1,457 patients who underwent OLT for FHF in the United States between 1988 and 2003 were enro

74 rge cohort of patients who underwent OLT for FHF was evaluated to develop and validate a system usefu

75 ct the probability of survival after OLT for FHF.

76 4 days) in the 3 patients undergoing OLT for FHF; in contrast, AA developed in the other 9 patients a

77 ical for devising therapeutic strategies for FHF.

78 and other nonsurgical medical therapies for FHF.

79 consecutive adult patients transplanted for FHF in an attempt to determine the extent of the histolo

80 reat benefit for the patients suffering from FHF.

81 Furthermore, FHF inhibited intrahepatic aspartate synthesis, which re

82 7 degrees C shortened survival time by half, FHF rats were not warmed during the postinduction period

83 of the homology core domain of all 10 human FHF isoforms.

84 tivity, contrary to the observation in human FHF.

85 taminophen overdose, a common cause of human FHF.

86 with a cyclosporine-based regimen (n=23) in FHF.

87 selective to the brain, may be of benefit in FHF.

88 and biochemical features seen clinically in FHF, including severely impaired ability of the residual

89 However, in FHF, c-kit mRNA levels were elevated in 3 of 6 specimens

90 map of metabolic alterations in the liver in FHF.

91 est c-kit staining, however, was observed in FHF, in which, in addition to the cells in the portal tr

92 We conclude that RI in FHF and RI requiring dialysis or liver-kidney transplant

93 These data suggest that in FHF patients who develop intracranial hypertension befor

94 The effect of an individual FHF on a specific VGSC varies greatly depending upon the

95 varies greatly depending upon the individual FHF isoform.

96 To induce FHF, rats were fasted for 36 hours, during which they re

97 ytic sites of fVIII biosynthesis by inducing FHF in mice using acetaminophen overdose, a common cause

98 is the treatment of choice for irreversible FHF, few investigations have examined pretransplant vari

99 lored fluorescent reporter system to isolate FHF and SHF progenitors from developing mouse embryos an

100 The approximately 500-kDa FHF complex contained all three Hook proteins, and small

101 inactivation, distal axonal Navs show little FHF association or FHF requirement for high-frequency tr

102 tatic factors in azoxymethane-induced murine FHF.

103 To examine this issue, we studied 50 NANB FHF patients and 104 liver transplant recipients from No

104 hepatitis B sequences in patients with NANB FHF may simply reflect geographic differences.

105 In contrast, all 9 non-FHF patients developing AA after OLT died, 5 due to infe

106 However, in the non-FHF patient, AA occurs in older individuals later in the

107 16 patients transplanted for other causes of FHF (11 paracetamol overdose, 2 idiosyncratic drug react

108 , all mild) transplanted for other causes of FHF.

109 nsistently displayed signs characteristic of FHF, including elevated plasma aminotransferase activity

110 nity is narrow for the dramatic condition of FHF, wide acceptance of this procedure will be of great

111 in teleosts, the primordial contributions of FHF and SHF to heart structure and function remain incom

112 considered in the differential diagnosis of FHF without clear etiology because of the potential for

113 ntification of a novel, conserved isoform of FHF-2 in chickens and mammals.

114 the characterization of multiple isoforms of FHF-1, -2, -3, and -4 which are generated through the us

115 rity to FGFs [3, 6, 7], but the mechanism of FHF action has not been reported.

116 developed and characterized a novel model of FHF in rats that has a number of physiological and bioch

117 pplemented by other tissues in this model of FHF.

118 The faster inactivation rate of FHF-free Navs together with very low axonal leak conduct

119 most patients succumbing to the sequelae of FHF before the correct diagnosis is made.

120 In the setting of FHF, it affects young males in the early posttransplanta

121 uld offer major benefits in the treatment of FHF.

122 ly creating new avenues for the treatment of FHF.

123 be beneficial in prevention and treatment of FHF.

124 l axonal Navs show little FHF association or FHF requirement for high-frequency transmission, velocit

125 We report that during an initial phase, FHF precursors differentiate rapidly to form a cardiac c

126 nd MELD score may be useful for prioritizing FHF-NA candidates.

127 Here we report bifluoride salts (Q(+)[FHF](-), where Q(+) represents a wide range of cations)

128 that loss of tbx5a and pitx2 affect relative FHF versus SHF contributions to the heart.

129 five patients (61%) grafted for seronegative FHF had fibrosis (13 mild, 9 moderate, and 3 severe) in

130 omplications, six patients with seronegative FHF required retransplantation (2 = chronic rejection; 1

131 mapped by two different groups: one studying FHF, the other studying a similar dominantly inherited s

132 We show here that FHF-1 is associated with the MAP kinase (MAPK) scaffold

133 We predict that FHF loss-of-function mutations would adversely affect cu

134 The FHF particle only blocks sodium channels from the open s

135 The FHF patients experienced more episodes of acute rejectio

136 Among the FHF patients, tacrolimus reduced the actuarial incidence

137 e identified a new multiprotein complex, the FHF complex, containing FTS, members of the microtubule-

138 delineate the functional contribution of the FHF and SHF to the zebrafish heart using the cis-regulat

139 er with the evolutionary conservation of the FHF isoforms among human, mouse, and chicken, these data

140 Members of the FHF subfamily share approximately 70% sequence identity,

141 lternative splicing of the first exon of the FHF-2 gene and is predicted to encode a polypeptide with

142 fever, as a prelude to identification of the FHF-susceptibility gene.

143 nts we identified a conserved surface on the FHF core domain that mediates channel binding in vitro a

144 ubdivisions of the heart tube (HT), with the FHF contributing the left ventricle and part of the atri

145 cardial drl reporter expression restricts to FHF descendants.

146 atic failure without acetaminophen toxicity (FHF-NA, n = 312) had the poorest survival probability wh

147 to activate FGFRs, suggesting that these two FHF residues contribute to the inability of FHFs to acti

148 thy based on altered Nav1.5 association with FHF proteins.

149 Patients who were diagnosed with FHF and admitted to the University of Chicago were eligi

150 ma in experimental models and in humans with FHF, an effect associated with normalization of CBF.

151 ostOLT mortality is higher for patients with FHF than for patients with other indications for OLT.

152 Patients with FHF unlikely to survive without liver transplantation we

153 rom plasma of blood donors and patients with FHF, and from blood products (factor VIII and IX clottin

154 For patients with FHF, the RI group had a lower patient survival rate at 1

155 s detected in four (19%) of 21 patients with FHF; in three cases, infection was detected at the onset