ライフサイエンスコーパス: SCAD

1 SCAD affects a young, predominantly female population, f

2 SCAD is a rare but challenging clinical entity.

3 SCADs that prevent neurodegenerative disorders, such as

4 The authors prospectively followed 327 SCAD patients.

5 oth the SCAD normal genetic background and a SCAD-deficient background.

6 /enhancer driving a mouse SCAD minigene (ALB-SCAD) on both the SCAD normal genetic background and a S

7 hs-cTnT with 1-year clinical outcomes among SCAD patients undergoing percutaneous coronary intervent

8 h, heart failure, myocardial infarction, and SCAD recurrence) was 47%.

9 ection significantly decreased both MCAD and SCAD expression, which is controlled by FoxA2.

10 ted cells rescued the expression of MCAD and SCAD.

11 -activated systemic platelets from STEMI and SCAD patients, 4 of which were selected for validation s

12 STEMI and SCAD samples were compared by a phosphoproteomics approa

13 Angiographic SCAD diagnosis was confirmed by 2 experienced interventi

14 Majority had type 2 angiographic SCAD (67.0%), only 29.1% had type 1, and 3.9% had type 3

15 romuscular dysplasia and type 2 angiographic SCAD.

16 Extreme exertion at SCAD onset was more frequent in men (7 of 16 versus 2 of

17 ved in another short-chain enzyme, bacterial SCAD.

18 The common SCAD polymorphisms may lead to clinically relevant alter

19 87 patients with angiographically confirmed SCAD.

20 Patients with confirmed SCAD (n=246; 45.3+/-8.9 years; 96% women) and 313 contro

21 ssion were used to produce the corresponding SCAD variant proteins.

22 n short-chain acyl-coenzyme A dehydrogenase (SCAD) from Megasphaera elsdenii.

23 d short-chain acyl coenzyme A dehydrogenase (SCAD), involved in the regulation of beta-oxidation of f

24 er of the short-chain alcohol dehydrogenase (SCAD) family of proteins.

25 Short chain acyl-CoA dehydrogenase (SCAD) is a homotetrameric flavoenzyme that catalyzes the

26 ion of a short-chain acyl-CoA dehydrogenase (SCAD) transgene in the SCAD-deficient mouse model.

27 icity in short chain acyl-CoA dehydrogenase (SCAD).

28 a group smoothly clipped absolute deviation (SCAD) regression procedure for selecting the TFs with va

29 and matched stable coronary artery disease (SCAD) controls in order to provide novel clues on the de

30 atients with stable coronary artery disease (SCAD) treated medically.

31 Spontaneous coronary artery dissection (SCAD) is a nonatherosclerotic acute coronary syndrome fo

32 Spontaneous coronary artery dissection (SCAD) is an acute coronary event of uncertain origin.

33 Spontaneous coronary artery dissection (SCAD) is an increasingly recognized nonatherosclerotic c

34 Spontaneous coronary artery dissection (SCAD) is gaining recognition as an important cause of my

35 Spontaneous coronary artery dissection (SCAD) is the most common cause of pregnancy-associated m

36 Spontaneous coronary artery dissection (SCAD) is underdiagnosed and an important cause of myocar

37 cted spontaneous coronary artery dissection (SCAD).

38 spital course, but 9 (10%) experienced early SCAD progression requiring revascularization.

39 tudy of 189 patients presenting with a first SCAD episode.

40 mmon in patients presenting with their first SCAD event (78% versus 17% in controls; P<0.0001; tortuo

41 In our large prospectively followed SCAD cohort, long-term cardiovascular events were common

42 serve as a marker or potential mechanism for SCAD.

43 PCI for SCAD is associated with high rates of technical failure

44 ly (n=134), 3 required revascularization for SCAD extension, and all 79 who had repeat angiogram >/=2

45 ues of the green wild-type, R147W, and G185S SCAD enzymes coexpressed with GroEL/ES were 33, 30, and

46 The proposed group SCAD regression procedure is very effective for identify

47 ty cardiac troponin T (hs-cTnT) elevation in SCAD patients undergoing elective percutaneous coronary

48 ine the prevalence of coronary tortuosity in SCAD and whether it may be implicated in the disease.

49 e found no detrimental effects of high liver SCAD expression in transgenic mice on either background.

50 months (interquartile range, 18-106 months), SCAD recurred in 15 patients, all female.

51 at albumin promoter/enhancer driving a mouse SCAD minigene (ALB-SCAD) on both the SCAD normal genetic

52 Multivessel SCAD was found in 23%.

53 s. 36%; p = 0.009), left main or multivessel SCAD (24% vs. 5%; p < 0.0001; and 33% vs. 14%; p = 0.002

54 n, Arg, and Lys and the wild type and mutant SCADs were produced in Escherichia coli and purified.

55 NA-SCAD survivors are at risk for recurrent cardiovascular

56 c spontaneous coronary artery dissection (NA-SCAD) is underdiagnosed and an important cause of myocar

57 Majority of patients with NA-SCAD had fibromuscular dysplasia and type 2 angiographic

58 Patients with NA-SCAD prospectively evaluated (retrospectively or prospec

59 prospectively evaluated 168 patients with NA-SCAD.

60 Nonatherosclerotic SCAD patients were prospectively followed at Vancouver G

61 Clinical predictors for recurrent de novo SCAD were tested using univariate and multivariate Cox r

62 dissection not associated with pregnancy (NP-SCAD).

63 ns and high-risk features than women with NP-SCAD did.

64 Compared with NP-SCAD, P-SCAD patients more frequently presented with ST-

65 nd they were compared with 269 women with NP-SCAD.

66 etion in urine, a clinical characteristic of SCAD deficiency.

67 The angiographic characteristics of SCAD are largely undetermined.

68 OCT ruled out the diagnosis of SCAD in 6 patients with coronary artery disease (atheros

69 There has been a surge in the diagnosis of SCAD in recent years, presumably due to an increased use

70 Angiographic features of SCAD are associated with extracoronary vasculopathy, inc

71 tion of hs-cTnT is observed in one fourth of SCAD patients undergoing elective percutaneous coronary

72 The majority of SCAD patients were taking aspirin and beta-blocker thera

73 rs, 9 female), OCT confirmed the presence of SCAD.

74 in-hospital outcomes, and long-term risk of SCAD recurrence or major adverse cardiac events were eva

75 Risks of SCAD recurrence and major adverse cardiac events in the

76 bstrate/product couple in the active site of SCAD.

77 regnant or </=12 weeks postpartum at time of SCAD.

78 ovide a comprehensive contemporary update of SCAD to aid health care professionals in managing these

79 P-SCAD patients had more acute presentations and high-risk

80 rred during the first postpartum month and P-SCAD patients less often had extracoronary vascular abno

81 ed spontaneous coronary artery dissection (P-SCAD) compared with spontaneous coronary artery dissecti

82 e for 323 women; 54 women met criteria for P-SCAD (4 during pregnancy) and they were compared with 26

83 The highest frequency of P-SCAD occurred during the first postpartum month and P-SC

84 Compared with NP-SCAD, P-SCAD patients more frequently presented with ST-segment

85 ith imaging of other vascular territories, P-SCAD was less likely with a diagnosis of fibromuscular d

86 nisms might be significant contributors to P-SCAD..

87 Compared with U.S. birth data, women with P-SCAD were more often multiparous (p = 0.0167), had a his

88 comprehensive retrospective and prospective SCAD data.

89 ty of Glu368 as the catalytic residue of rat SCAD and suggest that alteration of the position of the

90 hetical active site catalytic residue of rat SCAD, was replaced with Asp, Gly, Gln, Arg, and Lys and

91 n the SCAD-deficient background, recombinant SCAD activity and antigen in liver mitochondria were fou

92 Recurrent SCAD (n=40) occurred within segments of tortuosity in 80

93 Recurrent SCAD most often occurs within segments of tortuosity.

94 Recurrent SCAD occurred in 10.4% of patients.

95 Recurrent SCAD occurred in 13.1%.

96 ed (hazard ratio: 0.36; p = 0.004) recurrent SCAD.

97 arget vessel revascularization and recurrent SCAD were no different in revascularization versus conse

98 cardiovascular outcomes, including recurrent SCAD, are inadequately reported.

99 t cardiovascular events, including recurrent SCAD.

100 s associated with a higher risk of recurrent SCAD (hazard ratio, 3.29; 95% confidence interval, 0.99-

101 with a trend toward higher risk of recurrent SCAD (P=0.16).

102 Hypertension increased the risk of recurrent SCAD, whereas beta-blocker therapy appeared to be protec

103 comes and assess the predictors of recurrent SCAD.

104 target vessel revascularization or recurrent SCAD.

105 population and is associated with recurrent SCAD.

106 -term follow-up (median 2.3 years) recurrent SCAD occurred in 51 patients, with no difference in the

107 a mouse SCAD minigene (ALB-SCAD) on both the SCAD normal genetic background and a SCAD-deficient back

108 artery tortuosity is highly prevalent in the SCAD population and is associated with recurrent SCAD.

109 yl-CoA dehydrogenase (SCAD) transgene in the SCAD-deficient mouse model.

110 wo polymorphisms in the coding region of the SCAD gene, 511C>T (R147W) and 625G>A (G185S), have been

111 In three transgenic lines produced on the SCAD-deficient background, recombinant SCAD activity and

112 GPVI agonists in STEMI patients compared to SCAD controls.

113 The recombinant wild type SCAD kcat/K(m) values for butyryl-hexanoyl-, and octanoy

114 Among patients with SCAD (n=2029), 527 (26%) had elevated preprocedural hs-c

115 CT provides unique insights in patients with SCAD that allow an early diagnosis and adequate manageme

116 96% women) and 313 control patients without SCAD or coronary artery disease who underwent coronary a