ライフサイエンスコーパス: S.E.

1 x 10(-16)) and smoking status PRS (b = 0.05, S.E. = 0.005, p < 2 x 10(-16)) were found with their par

2 tween an individual's alcohol PRS (b = 0.05, S.E. = 0.006, p < 2 x 10(-16)) and smoking status PRS (b

3 with an IC(50) of 3.2 +/- 1 mum (mean +/- 1 S.E.; n = 6).

4 0.109 min(-1) S.E. 0.032, and 0.058 min(-1) S.E. 0.001 for LP1, NCIH929, and MOLP8 cell lines, respe

5 s of 0.239 min(-1) S.E. 0.076, 0.109 min(-1) S.E. 0.032, and 0.058 min(-1) S.E. 0.001 for LP1, NCIH92

6 measured CD38 K(int) values of 0.239 min(-1) S.E. 0.076, 0.109 min(-1) S.E. 0.032, and 0.058 min(-1)

7 currents over a 20-min period by 29% (+/-13 S.E., n = 5).

8 13.6 +/- 1.4 units/mg of protein (n = 22, +/-S.E.), whereas the A334T mutation yielded an enzyme with

9 0.2 nM S.E., n = 3) and SMPP-1M (5.9 +/- 1.3 S.E., n = 3).

10 Km for ATP of 680 +/- 226 microM (n = 3, +/-S.E.), the Michaelis constant for (RS)-mevalonate was in

11 >30-fold to 4623 +/- 1167 microM (n = 4, +/-S.E.) under standard assay conditions.

12 otal PCL-5 PTSD symptom count (beta = -0.43, S.E. = 0.23, z = -1.88, p < 0.06), and on the intrusions

13 he mean difference in signal ratios of 0.47 (S.E. 0.012, adjusted for clustering of observations with

14 ium current of hSkM1 channels by 190% (+/-54 S.E., n = 7) over a 20-min period.

15 1.94, p < 0.0525) and arousal (beta = -0.55, S.E. = 0.29, z = -1.92, p < 0.0552) clusters.

16 3.15, p = 0.0016) and arousal (beta = -0.56, S.E. = 0.26, z = -2.19, p < 0.0289, 95%CI[-1.07, -0.06])

17 ctional conductance (G(j)) of 1.16 nS+/-0.6 (S.E.), range 0.15-4.86 nS.

18 0.26 +/- 0.02 unit/mg of protein (n = 6, +/-S.E.), representing a decrease to 1.4% of control Vmax.

19 otal PCL-5 PTSD symptom count (beta = -0.65, S.E. = 0.32, z = -2.04, p = 0.041, 95%CI[-1.27, -0.03]),

20 lated to baseline predictors (AU-ROC = 0.68, S.E. = 0.01), with test sample outcome prevalence of 32.

21 elihood methods suggests they spent 60.7 +/- S.E. 7.5 days in Fuvahmulah, with a larger aggregation s

22 0.06), and on the intrusions (beta = -0.73, S.E. = 0.38, z = -1.94, p < 0.0525) and arousal (beta =

23 rations in cognition and mood (beta = -0.85, S.E. = 0.27, z = -3.15, p = 0.0016) and arousal (beta =

24 decreased LKB1 kinase activity by 31 +/- 9% (S.E.) but had no effect on the association of LKB1 with

25 34.9 +/- 1.9 pmol/mg of protein/min (chi +/- S.E.; n = 10).

26 The Staphylococcus aureus enterotoxins (S.E.) A-I, and toxic-shock syndrome toxin TSST-1 act as

27 search Institute for Scientists Emeriti (R.I.S.E.) at Drew University have been very rewarding and ar

28 should be described by confidence intervals; S.E. should not be used.

29 We calculated a mean (+/-S.E.) collagen half-life of 197.53 (+/-18.23) years for

30 s of normal BDCCs to 1.20 +/- 0.01 (mean +/- S.E., n = 50) in 10 min, followed by RVD to 1.07 +/- 0.0

31 trans- Golgi pH was 6.25 +/- 0.04 (mean +/- S.E.; n = 80, vector control), 6.30 +/- 0.03 (n = 74, CF

32 control for each set, of 0.99-4.18 (mean +/- S.E., 1.94 +/- 0.404), 1.0-5.24 (2.11 +/- 0.51), and 0.9

33 versus 82 +/- 8% inhibition; n = 4 (mean +/- S.E.), respectively).

34 eomycin controls (p < 0.001, n = 5, mean +/- S.E.).

35 ease CAT activity by 45.4 +/- 7.9% (mean +/- S.E., n = 8).

36 .003 cm/s observed at 20 degrees C (mean +/- S.E.; n = 15).

37 versus 1.8 +/- 0.13 pmol/oocyte/h, mean +/- S.E., p < 0.05).

38 compared with 100.5 +/- 0.8 mm Hg (mean +/- S.E., n = 18) for control mice.

39 or one line and 88.8 +/- 1.6 mm Hg (mean +/- S.E., n = 19, P < 0.001) for another, as compared with 1

40 genic mice were 88.5 +/- 0.8 mm Hg (mean +/- S.E., n = 19, P < 0.001) for one line and 88.8 +/- 1.6 m

41 150 +/- 23 and 440 +/- 190 microM (mean +/- S.E.) for substrates (RS)-mevalonate and ATP, respective

42 l thickness in vivo was (in microm, mean +/- S.E., n = 5 mice) 123 +/- 1 (wild type), 101 +/- 2 (AQP1

43 25.1 +/- 1.8 and 32.2 +/- 2.5 min (mean +/- S.E.), respectively.

44 0 min in insulin-stimulated muscle; mean +/- S.E.).

45 r cell with a Kd of 3.7 +/- 1.4 nM (mean +/- S.E., n = 9).

46 1 versus 2056 +/- 83 mosM/kg H(2)O, mean +/- S.E., p < 0.001).

47 duced to 6.0 +/- 0.6% by PKGIalpha (mean +/- S.E., n = 7, p < 0.001).

48 uced to 18.6 +/- 0.8% by PKGIalpha (mean +/- S.E., n = 7, p < 0.001).

49 s 13.4 +/- 0.8 ng/ml, respectively (mean +/- S.E.)).

50 IC(50) mean+/-S.E. for spike rates was 5.4+/-0.7 microM (n=15).

51 en non-stroke (372+/-23% of baseline, mean+/-S.E.) and stroke sides (383+/-30%) in Group 1.

52 baseline diameter=94+/-5 micrometers, mean+/-S.E.) were measured using a closed cranial window in ane

53 eeding rate was 2.0+/-0.37 bites/min (mean+/-S.E.).

54 Gj was 1.52+/-0.29 nS (mean+/-S.E.; n=147).

55 In young animals, NE release (mean+/-S.E., pg/min) was 4.0+/-1.1 pg/min at 1300 h and increas

56 by 30, or 60 min of reperfusion, the Mean+/-S.E. (n=5) percentage of maximal cTnI release was 30 +/-

57 ation was rapid (t((1)/(2)), 7.3 +/- 0.4 ms, S.E., n = 11 mice) and blocked by acetazolamide and incr

58 wn in three different locations near Murcia (S.E. Spain) has been studied.

59 Muller cells (-64 +/- 1 versus -64 +/- 1 mV, S.E., n = 24).

60 0.6 nM S.E., n = 3), PP-2AC (0.63 +/- 0.2 nM S.E., n = 3) and SMPP-1M (5.9 +/- 1.3 S.E., n = 3).

61 the nM range against PP-1C (1.58 +/- 0.6 nM S.E., n = 3), PP-2AC (0.63 +/- 0.2 nM S.E., n = 3) and S

62 We show that the S.E. Australian wildfires are the cause of this lower st

63 complexity grading scale for ERCP-the H.O.U.S.E.-classification.

64 ontained (in units of mmol/kg dry weight +/- S.E.) large amounts of phosphorus (1390 +/- 13), magnesi