ライフサイエンスコーパス: FBD

1 FBD for anastomotic strictures after esophageal atresia

2 FBD is associated with a point mutation in the stop codo

3 FBD is caused by a missense mutation at the stop codon o

4 FBD was successful in 93 patients (90%): 44 (47%) after

5 FBD(KI) mice are a model of FBD that is genetically cong

6 FBDs were less common in older individuals, and all exce

7 tients (61 male patients, 59%) underwent 378 FBD sessions (median, two dilations per patient; range,

8 esophageal perforations (1%) developed after FBD.

9 do not necessarily negate a diagnosis of an FBD.

10 anslational processing of wild type BRI2 and FBD-BRI2 result in the production of a 23-residue long B

11 alyzed glutamatergic transmission in FDD and FBD knock-in mice, which carry pathogenic FDD and FBD mu

12 Collectively, the data show that FDD and FBD mutations cause a reduction of BRI2 levels and funct

13 nock-in mice, which carry pathogenic FDD and FBD mutations into the mouse endogenous Itm2b gene.

14 ptides have been proposed to mediate FDD and FBD pathogenesis by impairing synaptic Long-term potenti

15 ts in the neuronal damage leading to FDD and FBD, respectively.

16 to dementia and neurodegeneration in FDD and FBD.

17 ly exclusive, have been proposed for FDD and FBD: 1) loss of BRI2 function; 2) accumulation of amyloi

18 pathogenic mechanism common to AD, FDD, and FBD.

19 al British dementia with amyloid angiopathy (FBD) is an autosomal dominant condition characterized by

20 l the formation of dynamic complexes between FBD and cyt c on a fast exchange time scale.

21 ctron transfer and complex formation between FBD and cyt c are investigated.

22 ably, BRI2 mutations cause familial British (FBD) and Danish dementias (FDD) that are clinically and

23 athology and clinical presentation shared by FBD and Alzheimer disease (AD) have led some to suggest

24 apid in vivo functional testing of candidate FBD genes.

25 lly recognized leaders in basic and clinical FBD research.

26 y be an opportunity to improve comprehensive FBD management because fewer than 1 in 5 ambulatory visi

27 When compared with full-length CPR, FBD reduces cyt c at a higher rate in both the semiquino

28 We introduce the "fossilized birth-death" (FBD) process--a model for calibrating divergence time es

29 ur primary outcome, facility-based delivery (FBD), and time period, defined as the pre-EVD period (Ma

30 ome 13 dementias, familial British dementia (FBD) and familial Danish dementia (FDD), are associated

31 onditions, termed familial British dementia (FBD) and familial Danish dementia (FDD).

32 Familial British dementia (FBD) is a rare neurodegenerative disorder and shares fea

33 Familial British dementia (FBD) is an autosomal dominant neurodegenerative disorder

34 Familial British dementia (FBD) is an early onset inherited disorder that, like fam

35 Familial British dementia (FBD) is an inherited neurodegenerative disease believed

36 Familial British Dementia (FBD) is caused by an autosomal dominant mutation in the

37 lesion underlying familial British dementia (FBD), an autosomal dominant neurodegenerative disorder,

38 mer disease (AD), familial British dementia (FBD), and familial Danish dementia (FDD), are caused by

39 Familial British dementia (FBD), previously designated familial cerebral amyloid an

40 cause familial British and Danish dementia (FBD and FDD), autosomal dominant disorders characterized

41 cause familial British and Danish dementia (FBD and FDD).

42 al model based on a fractional bulk density (FBD) concept was presented for estimating soil water ret

43 al and regional burden of foodborne disease (FBD), the World Health Organization (WHO) established th

44 Foodborne diseases (FBDs) are a major cause of morbidity and mortality in th

45 Diagnosis of a functional bowel disorder (FBD) requires characteristic symptoms during the last 3

46 al treatments in functional bowel disorders (FBD) are methodologically limited.

47 understanding of functional bowel disorders (FBD) is critical as they impose a negative economic impa

48 Heritable fragile bone disorders (FBDs), ranging from multifactorial to rare monogenic con

49 (IBS) and other functional bowel disorders (FBDs) are prevalent disorders with altered microbiota.

50 Functional bowel disorders (FBDs) are the most common gastrointestinal problems mana

51 tions of Rome IV functional bowel disorders (FBDs) or their effects on quality of life.

52 ecially true for functional bowel disorders (FBDs), a heterogeneous and challenging group of syndrome

53 ed a workshop on functional bowel disorders (FBDs), particularly irritable bowel syndrome, with the o

54 istinct from the functional bowel disorders (FBDs).

55 domains, among which the FMN binding domain (FBD) is the direct electron donor to cyt c.

56 nd 4.1/ezrin/radixin/moesin) binding domain (FBD) whose mammalian binding partners are not well under

57 enerated a knock-in (KI) mouse model of FBD (FBD(KI)) genetically congruous with the human disease.

58 The median age at first FBD was 2.2 years (range, 0.1-19.5 years).

59 fish crispant screening as a robust tool for FBD gene validation, combining skeletal and molecular an

60 d a need to revise the Rome III criteria for FBDs, last published in 2006.

61 ral population meet the Rome IV criteria for FBDs.

62 of the amyloid subunit (ABri) extracted from FBD brain tissues is entirely different and unrelated to

63 Electron transfer from FBD to cyt c occurs at distinct rates that are dependent

64 GE-FBD may provide an alternative to rapidly search for com

65 tically encoded fragment-based discovery (GE-FBD) uses selection of phage-displayed glycopeptides to

66 ion of mature BRI2 in both KI mice and human FBD brains.

67 In FBD patients, the ABri peptide is produced as a result o

68 ferences among the amyloid subunits (ABri in FBD, ADan in FDD, and Abeta in AD), these disorders are

69 ted stratified analyses to assess changes in FBD by whether respondents believed that health facility

70 d with severe hippocampal memory deficits in FBD(KI) mice.

71 tides that accumulate in amyloid deposits in FBD brain.

72 be the main component of amyloid deposits in FBD brains.

73 ize both parenchymal and vascular lesions in FBD patients.

74 The reduction in FBD during the EVD period was observed among those repor

75 iciency prevents memory dysfunctions seen in FBD(KI) mice.

76 present memory deficits similar to those in FBD(KI) animals.

77 cified FBDs, and 28.6%-31.7% for any Rome IV FBD.

78 prevalence values of census-adjusted Rome IV FBDs were similar among the 3 countries; ranges were: 4.

79 at the stop codon of the BRI2 gene and, like FBD patients, FBD(KI) mice carry this mutation in one of

80 bridge formation between Glu-213/Glu-214 of FBD and Lys-87 of cyt c, which may be essential for the

81 analysis of plaques and vascular amyloid of FBD brains revealed that a 4 kDa peptide named ABri is t

82 The global burden of FBD caused by the 31 hazards in 2010 was 33 million Disa

83 Thus, the burden of FBD is borne particularly by children under five years o

84 We find that the global burden of FBD is comparable to those of the major infectious disea

85 ality, had considerably different burdens of FBD, with the greatest falling on the subregions in Afri

86 Other major causes of FBD deaths were Salmonella Typhi, Taenia solium and hepa

87 hoidal S. enterica, were important causes of FBD in all regions of the world, whereas others, such as

88 However, pathological examination of FBD brains has shown the presence of ABri as non-fibrill

89 Immunohistochemistry of FBD and FDD brain sections demonstrated the presence of

90 we generated a knock-in (KI) mouse model of FBD (FBD(KI)) genetically congruous with the human disea

91 FBD(KI) mice are a model of FBD that is genetically congruous to the human disease,

92 We detected a 30% decreased odds of FBD after the start of EVD in a rural Liberian county wi

93 contributing factor for the pathogenesis of FBD and FDD and, in more general terms, to other neurode

94 play a critical role in the pathogenesis of FBD and suggest that a similar process may also operate

95 s play a central role in the pathogenesis of FBD.

96 c peptides that initiate the pathogenesis of FBD.

97 Limitations include the possibility of FBD secular trends coincident with the EVD period, recal

98 hemical shift mapping identified residues of FBD involved in the binding interface with cyt c, most o

99 Eleven individuals at risk of FBD, aged between 44 and 56 years, agreed to undergo a c

100 es that are dependent on the redox states of FBD.

101 r residues distributed around the surface of FBD.

102 Toronto with moderate to severe symptoms of FBD.

103 Subanalyses were performed for type of FBD and dose, type, and duration of prebiotic.

104 initiative to estimate the global burden of FBDs in terms of Disability Adjusted Life Years (DALYs).

105 Accurate information on the burden of FBDs is needed to inform policy makers and allocate appr

106 inning the heterogeneous lived experience of FBDs.

107 to better understand the lived experience of FBDs.

108 s to identify risk and protective factors of FBDs, identification of biomarkers and endophenotypes in

109 Treatment of FBDs is based on an individualized evaluation, explanati

110 pathophysiology, diagnosis and treatment of FBDs.

111 an urgent need for improved understanding of FBDs.

112 d trials (RCTs) in adults with IBS and other FBDs.

113 otics to placebo in adults with IBS or other FBDs were included.

114 ymptoms or QoL in patients with IBS or other FBDs, but they do increase bifidobacteria.

115 don of the BRI2 gene and, like FBD patients, FBD(KI) mice carry this mutation in one of the two murin

116 ) in female patients with moderate to severe FBD (irritable bowel syndrome, functional abdominal pain

117 For female patients with moderate to severe FBD, CBT is effective and DES may be effective when take

118 its paralog, Kss1; a second activator (Ste5-FBD) that tunes mating behavior is, in contrast, not con

119 clinic visits alone for chronic symptomatic FBDs is approximately US$358 million (95% CI, 233-482 mi

120 The management of chronic symptomatic FBDs is associated with considerable health care resourc

121 to assess the burden of chronic symptomatic FBDs on ambulatory care delivery in the United States an

122 employed physicians for chronic symptomatic FBDs were sampled.

123 Moreover, the FBD model allows for inclusion of all available fossils.

124 The structural model of the FBD-cyt c complex indicates two possible orientations of

125 Results showed that the FBD model was effective for all soil textures and bulk d

126 and show that node age estimation under the FBD model results in robust and accurate estimates of sp

127 This manuscript classifies the FBDs into five distinct categories: irritable bowel synd

128 Third, FBDs are broadly accepted as bidirectional disorders of

129 Thus, FBD constitutes the first documented cerebral amyloidosi

130 esponsible for the majority of deaths due to FBD.

131 g/distention (FAB/D); and unspecified FBD (U-FBD).

132 s for 103 consecutive patients who underwent FBD with our interventional radiology service (1999-2011

133 bloating/distention (FAB/D); and unspecified FBD (U-FBD).

134 pain, painful constipation, and unspecified FBD).

135 ced constipation, 7.5%-10.0% for unspecified FBDs, and 28.6%-31.7% for any Rome IV FBD.

136 deposited in the brains of individuals with FBD.

137 Patients with FBD have a single nucleotide substitution at codon 267 i

138 Subjects with FBD had significant reductions in quality of life and re

139 nd impact on quality of life associated with FBDs necessitate an urgent need for improved understandi

140 Clinical assessment of patients with FBDs should be less concerned with diagnostic classifica