ライフサイエンスコーパス: normal control group

1 s (at least r=0.76, P<0.0001) but not in the normal control group.

2 n girls with other disorders or those in the normal control group.

3 in myopic eyes compared with an age-matched normal control group.

4 gnificant correlations were found within the normal control group.

5 h hippocampal damage (moderate/severe) and a normal control group.

6 were similar in the two study groups and the normal control group.

7 r atrophy group diminished compared with the normal control group.

8 he LND patients was observed compared to the normal control group.

9 roup of subjects with SQCP aged 2-18 y and a normal control group.

10 h "moderate" hippocampal damage (MHD), and a normal control group.

11 iduals with primary RLS and a neurologically normal control group.

12 miliar and stranger faces in both autism and normal control groups.

13 ve aphasia, along with neurodegenerative and normal control groups.

14 POE4 non-carriers (group 2, n = 29), and AB- normal controls (group 0, n = 129).

15 l controls (normal control group ] [NC1] and normal control group 2 [NC2]) (n = 14 for each).

16 exposure of the liver: group 1 (n = 7) were normal controls; group 2 (n = 7) had hepatic fibrosis.

17 ed into three groups (group 1: Sham-operated normal controls; group 2: Ischemia-reperfusion injury wi

18 ly affected families, their relatives, and a normal control group (214 subjects).

19 d into three groups based on DR severity and normal control group: 39 eyes no DR, 64 eyes NPDR, 33 ey

20 her in the group with CP (85.7%) than in the normal control group (73.3%; P <0.03).

21 sponse to hypoglycemia between the H and the normal control group after fasting for 48 h (H 29,639 +/

22 voxel [(18)F]dopa K(i)(o) values between the normal control group and each Parkinson's disease group

23 ntly lower cortisol levels than girls in the normal control group at all 3 sampling times.

24 evation in both the patient group and in the normal control group, but no evidence of a differential

25 whereas it decreased in glaucoma control and normal control groups by 2.0 mm Hg (P = .003) and 2.1 mm

26 wley rats into three groups: group N was the normal control; group C was given 40 mg/kg body weight p

27 The normal control group exhibited clot times of 5.7+/-0.3 m

28 ed significantly from that in the stroke and normal control groups, giving an odds ratio of 2.51 (95%

29 n pattern in five patients compared with the normal control groups; in all five patients this atypica

30 were significantly lower in IDCM than in the normal control group (MFAU: 134 +/- 44 vs. 213 +/- 49 nm

31 U were significantly higher in IDCM than the normal control group (MGU: 247 +/- 63 vs. 125 +/- 64 nmo

32 A normal, control group (n = 15) was given vehicle and not

33 on with 2 groups of matched normal controls (normal control group ] [NC1] and normal control group 2

34 7 in the RA group, compared with 0.86 in the normal control group (P = 0.0002 for both).

35 Compared to a CAG-normal control group, the CAG-expanded group demonstrate

36 Comparing with the normal control group, the GM and WM density at each leve

37 represented the control groups, namely, the normal control group, the S. mansoni-infected control gr

38 patients with and without limb apraxia and a normal control group to examine preprogramming and respo

39 myopic subjects compared with an age-matched normal control group using ultra widefield optical coher

40 system atrophy patients as compared with the normal control group, with average reductions of 61% in