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

7 esophageal perforations (1%) developed after FBD.

8 do not necessarily negate a diagnosis of an FBD.

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

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

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

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

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

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

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

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

17 lly recognized leaders in basic and clinical FBD research.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

37 istinct from the functional bowel disorders (FBDs).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

52 tides that accumulate in amyloid deposits in FBD brain.

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

54 ize both parenchymal and vascular lesions in FBD patients.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

74 c peptides that initiate the pathogenesis of FBD.

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

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

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

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

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

80 r residues distributed around the surface of FBD.

81 Toronto with moderate to severe symptoms of FBD.

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

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

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

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

86 pathophysiology, diagnosis and treatment of FBDs.

87 an urgent need for improved understanding of FBDs.

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

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

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

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

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

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

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

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

96 Third, FBDs are broadly accepted as bidirectional disorders of

97 Thus, FBD constitutes the first documented cerebral amyloidosi

98 esponsible for the majority of deaths due to FBD.

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

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

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

102 pain, painful constipation, and unspecified FBD).

103 deposited in the brains of individuals with FBD.

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

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