ライフサイエンスコーパス: CVA

1 CVA estimates those multivariate patterns of activation

2 CVA is a physiological phenomenon of importance to healt

3 dex (h(s)2 = 0.212, SE = 0.1347, P = 0.0611; CVA = 0.1826).

4 ienced CVAs, as compared with 3 deaths and 9 CVAs in the 25 patients who remained on intensified anti

5 A CVA occurred in 92 patients (0.30% of procedures).

6 A CVA was defined as a composite of transient ischemic att

7 with the experimental design; the order of a CVA model is then determined by the number of significan

8 failure (CHF), or cerebrovascular accident (CVA) from 1991 to 1994.

9 s had at least one cerebrovascular accident (CVA) in follow-up; 35 patients had at least one CVA or t

10 and prevalence of cerebrovascular accident (CVA) in paced versus unpaced patients during admission t

11 gher prevalence of cerebrovascular accident (CVA) in patients with SEC when compared with controls wi

12 Cerebrovascular accident (CVA) is a major complication of sickle cell disease.

13 irst occurrence of cerebrovascular accident (CVA) or death.

14 CVIs, freedom from cerebrovascular accident (CVA) or transient ischemic attack (TIA), and 30-day mort

15 ication were prior cerebrovascular accident (CVA), chronic obstructive pulmonary disease (COPD), type

16 d occlusion, prior cerebrovascular accident (CVA), or SPs less than 35 mmHg.

17 tive/postoperative cerebrovascular accident (CVA), postoperative bleeding, and sternal wound infectio

18 nfarction (MI), or cerebrovascular accident (CVA).

19 arctions (MI) and cerebrovascular accidents (CVA) in patients with diabetic macular edema (DME) compa

20 </= 70 years from cerebrovascular accidents (CVA) or trauma that were correlated with eligible deaths

21 l implications of cerebrovascular accidents (CVAs) after percutaneous coronary interventions (PCIs).

22 t visual acuity (LCVA), color visual acuity (CVA), and visual fields (VF).

23 24 months by traditional increment analysis (CVA & FOTI at the D(3) (dentin only) threshold + radiogr

24 t controls using Canonical Variate Analysis (CVA) provides several distinct clusters for each scenari

25 lution based on Canonical Variates Analysis (CVA) model scoring at the subject level and random effec

26 On multivariate analysis, CVA was independently associated with in-hospital death

27 (ANOVA) approach, report on the analytical (CVA), intraindividual (CVI), and between individual (CVG

28 Increase of isolation of EV-A71 and CVA--the predominant pathogens for the hand, foot, and m

29 e frequencies of hospitalization for AMI and CVA did not differ from those of the comparison group, b

30 ubstantially increased risk of AMI, CHF, and CVA.

31 t hypothermia and normoxia, TVR was high and CVA unit activity was present, with marked respiratory m

32 ntrast, during hyperthermia, TVR was low and CVA unit activity was absent.

33 adjusted rate ratios of hospitalized MI and CVA events were then calculated.

34 decrease of >/= 7 mum predicted poor VF and CVA (sensitivity of 78% and 100% and specificity of 63%

35 innervating the caudal ventral tail artery (CVA) of anaesthetised rats can still be recorded followi

36 units supplying tail caudal ventral artery (CVA) in spontaneously breathing anaesthetized rats, whil

37 was assessed by clinical visual assessment (CVA-simplified version of Dundee Selectable Threshold Me

38 least one CVA or transient ischemic attack (CVA/TIA).

39 employed in cerebrovascular autoregulation (CVA) tests on the brain, without contact and in real tim

40 migration along the mouse crypt-villus axis (CVA).

41 ere in sickle cell anemia (SS) patients, but CVA occurred in all common genotypes.

42 th Fast Fourier Transform (FFT), followed by CVA treatment.

43 e assay was compared with culture on a Campy-CVA plate (Remel, Lenexa, Kans.) and blood-free campylob

44 A prognostic risk score (CARRS [CVA, albumin, re-HTx, renal dysfunction, and sternotomie

45 P; deaths from CVA: 34-118 PMP; and combined CVA and trauma: 91-229 PMP.

46 nd contralateral vestibuloacoustic efferent (CVA) neurons are incorrectly specified.

47 treatment, 1 patient died and 2 experienced CVAs, as compared with 3 deaths and 9 CVAs in the 25 pat

48 ntly associated with actuarial rate of first CVA included hypertension (P = .002), age (P < .0001), c

49 o 2.37) for CVA and 1.68 (1.003 to 2.06) for CVA/TIA.

50 ncidence ratios were 1.74 (0.94 to 2.37) for CVA and 1.68 (1.003 to 2.06) for CVA/TIA.

51 to 2.46) for MI, 1.28 (CI, 1.06 to 1.54) for CVA, and 2.13 (CI, 1.61 to 2.81) for PVD.

52 isk per 1,000 patients per year was 1.67 for CVA and 2.76 for CVA/TIA.

53 ients per year was 1.67 for CVA and 2.76 for CVA/TIA.

54 idence and mortality of and risk factors for CVA in sickle cell disease patients in the United States

55 1-1.49), and the risk of hospitalization for CVA was not significantly different from those in the co

56 HR for MI, 11.89 [CI, 2.40 to 59.00]; HR for CVA, 3.93 [CI, 1.76 to 8.79]; HR for PVD, 3.86 [CI, 0.78

57 The adjusted rate ratio for CVA was 1.98 (95% CI: 1.39-2.83, p < 0.001) for DME vers

58 lar assist device patients at major risk for CVA and death.

59 OPOs: trauma deaths: 44-118 PMP; deaths from CVA: 34-118 PMP; and combined CVA and trauma: 91-229 PMP

60 The 1-year freedom from CVA or death was 87.5% and 49.5% in the surgical and med

61 sis, there was no difference in freedom from CVA or TIA for the 2 groups (P = .07).

62 ion, but there were no consistent changes in CVA unit firing rate or T-rhythm frequency, although res

63 The incidence of infarctive CVA was lowest in SS patients 20 to 29 years of age and

64 There were 19 ipsilateral CVAs (2.7%).

65 s is associated with increased risks for MI, CVA, and PVD.

66 n age, 73 years), the incidence rates of MI, CVA, and PVD were 10.0, 8.0, and 4.2 events per 1000 per

67 lyses were conducted for the outcomes of MI, CVA, and PVD.

68 In wild-type mice CVA neurons migrate from r4 into the contralateral side,

69 es more likely to be hospitalized because of CVA (95% CI 1.17-2.93).

70 n independent and more powerful correlate of CVA than reduced LAAEV or atrial size.

71 mia, Charlson comorbidity scores, history of CVA, hyperlipidemia, and other cerebrovascular diseases.

72 e of anticoagulation and higher incidence of CVA.

73 Age was the only significant predictor of CVA alone (P < .001).

74 Predictors of CVA events were cardiac arrhythmia, Charlson comorbidity

75 P = .003) remained significant predictors of CVA/TIA.

76 The highest rates of prevalence of CVA (4.01%) and incidence (0.61 per 100 patient-years) w

77 patients with SEC had a higher prevalence of CVA than controls, p = 0.03.

78 SR is associated with a higher prevalence of CVA.

79 The rate of CVA or TIA in the iBCVI group was 5.1% compared with 15.

80 e-specific prevalence and incidence rates of CVA in patients with the common genotypes of sickle cell

81 matologic and clinical events on the risk of CVA were analyzed.

82 seline hypertension led to increased risk of CVA/TIA (log-rank P < .0001).

83 ) in follow-up; 35 patients had at least one CVA or transient ischemic attack (CVA/TIA).

84 Event rates of MI or CVA were higher in patients with DME than in diabetes co

85 ated with an increased risk of death, MI, or CVA compared with patients who were aspirin sensitive (2

86 Among them, 19 had clinically overt CVA, 20 had life-threatening hypoxic episodes or soft ne

87 ient (FSIQ) was associated with either overt CVA or silent ischemic lesions.

88 Among the 30 subjects with no overt CVA, 25 (83%) demonstrated imaging abnormalities based o

89 Of the 19 subjects with overt CVA, 17 had abnormal MRI (89%), 17 had abnormal PET (89%

90 cteristics of those who had a periprocedural CVA were compared with those who did not.

91 s ratio [OR], 1.16; P=.261) or postoperative CVA (adjusted OR, 1.06; P=.765), risks of sternal wound

92 1.9, 95% CI 1.1 to 3.3; p = 0.033), previous CVA (OR 2.3, 95% CI 1.3 to 4.0; p = 0.0059), and creatin

93 The prevalence of prior CVA was not significantly different between the three gr

94 arin is contraindicated and history of prior CVA was studied in three groups: 1) group A with continu

95 ) there was recommencement of firing in some CVA units, at low discharge rate, with respiratory modul

96 risk for cerebral vasculopathy with stroke (CVA) and cognitive impairment.

97 ession of lineage-specific markers along the CVA consistent with transcription site repression of the

98 the normal reprogramming of cells along the CVA was dampened in the Apc(1638N/+) mice, with an overr

99 mutants, motor neurons differentiate but the CVA and FBM neurons fail to migrate into their proper po

100 flow and vascular resistance (TVR) from the CVA, under conditions of modest hypothermia and hyperthe

101 xia in TVR and sympathetic nerve activity to CVA are dependent on core temperature.

102 This approach can also be applied to CVA models with a fixed number of canonical vectors but

103 Of the 15 total CVAs or TIAs, 11 (73.3%) resulted from carotid injury an

104 s suggest acceptable analytical variability (CVA < or = 1/2 CVI) for all assays.

105 , SEC in NSR was found to be associated with CVA, larger LA size and decreased mean LAAEV.

106 Factors associated with CVA/TIA were hypertension (P < .001), coronary artery di

107 olution of a primary hemolysis event without CVA or death occurred in 21/24 patients treated with sur