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1 CVA estimates those multivariate patterns of activation
2 CVA is a physiological phenomenon of importance to healt
4 ienced CVAs, as compared with 3 deaths and 9 CVAs in the 25 patients who remained on intensified anti
7 with the experimental design; the order of a CVA model is then determined by the number of significan
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
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
17 tive/postoperative cerebrovascular accident (CVA), postoperative bleeding, and sternal wound infectio
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).
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
27 (ANOVA) approach, report on the analytical (CVA), intraindividual (CVI), and between individual (CVG
29 e frequencies of hospitalization for AMI and CVA did not differ from those of the comparison group, b
31 t hypothermia and normoxia, TVR was high and CVA unit activity was present, with marked respiratory m
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
39 employed in cerebrovascular autoregulation (CVA) tests on the brain, without contact and in real tim
43 e assay was compared with culture on a Campy-CVA plate (Remel, Lenexa, Kans.) and blood-free campylob
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
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
59 OPOs: trauma deaths: 44-118 PMP; deaths from CVA: 34-118 PMP; and combined CVA and trauma: 91-229 PMP
62 ion, but there were no consistent changes in CVA unit firing rate or T-rhythm frequency, although res
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
71 mia, Charlson comorbidity scores, history of CVA, hyperlipidemia, and other cerebrovascular diseases.
80 e-specific prevalence and incidence rates of CVA in patients with the common genotypes of sickle cell
85 ated with an increased risk of death, MI, or CVA compared with patients who were aspirin sensitive (2
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
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
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
107 olution of a primary hemolysis event without CVA or death occurred in 21/24 patients treated with sur
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