ライフサイエンスコーパス: S.E.M.

1 5 (S.E.M.) muM and V(max) of 0.03 +/- 0.002 (S.E.M.) nmol/mg of protein/min.

2 collaterals (0.082 spines/microns +/- p.021 S.E.M.).

3 zure frequency of 0.11 seizures/day +/- 0.03 S.E.M. in 30 animals.

4 not change with age; it was 1.07 +/- 0.037 (S.E.M.) in males and 1.08 +/- 0.022 cm2 in females.

5 was shorter in these cells (14.2 ms +/- 2.1 S.E.M., P < 0.01) compared with normal DGCs in control a

6 ped dendritic domain of 54.1 degrees +/- 4.1 S.E.M. with 13.8 +/- 1.1 branch points and an estimated

7 alculated to be 0.25 spines/microns +/- 0.16 S.E.M..

8 s in wild-type control mice was 0.47+/-0.19 (S.E.M.) m/s (n=5), similar to the conduction velocity re

9 ritic region (0.750 spines/microns +/- 0.203 S.E.M.: P < 0.01) than the DGCs without such collaterals

10 ntly increased to 2.57 seizures/day +/- 0.25 S.E.M. (ranging from 2-13 seizures/day) in 40-165 days,

11 tween sexes (P = 0.676) supine (-281 +/- 46 (S.E.M.) units beat(-1) mmHg(-1) in men vs -252 +/- 52 in

12 of DDP with an apparent K(m) of 1.2 +/- 0.5 (S.E.M.) muM and V(max) of 0.03 +/- 0.002 (S.E.M.) nmol/m

13 ) reduction in brain infarct volume and 50% (S.E.M.=0.48) reduction in the neurological evaluation sc

14 mal DGCs in control animals (21.2 ms +/- 3.7 S.E.M.) suggesting that cell structural diminution possi

15 Animals treated with NAC showed a 49.7% (S.E.M.=1.25) reduction in brain infarct volume and 50% (

16 n volume of the male brain was 89.2 +/- 1.9 (S.E.M.) compared to the female brain volume of 70.8 +/-

17 Twenty-three subjects with a mean (S.E.M.) age of 28 (1.5) years took part in the study.

18 Mean (+/- S.E.M.) baseline heart rates and arterial pressures were

19 Mean (+/- S.E.M.) heart rates before lower body suction were simil

20 In 20 frog capillaries, mean (+/- S.E.M.) P(S) (in microm s(-1)) = 9.35 (+/- 1.55)U x 10(-

21 Prior to exercise mean (+/- S.E.M.) BRS was 10.92 +/- 6.3 ms mmHg(-1), and BRS remai

22 As in previous studies, mean (+/- S.E.M.) stroke volume was lower (46 +/- 5 vs. 76 +/- 3 m

23 dent measurements of 0.34 +/- 0.01 (mean +/- S.E.M., n = 16).

24 amplitude (228 +/- 51%; P < 0.05) (mean +/- S.E.M.) and duration of the lung bursts (3.5 +/- 0.1 to

25 ernation amplitude, 1.23 +/- 0.07% (mean +/- S.E.M.); etCO2, 7.56 +/- 0.15%) over 2-8 s at two Pa,O2

26 5.8 +/- 4.8 mmol (kg dry weight)-1 (mean +/- S.E.M.) and 93.1 +/- 14.1 mmol (kg dry weight)-1, respec

27 x 10(-6) +/- 0.247 x 10(-6) cm s-1 (mean +/- S.E.M.) at 0.25 mM, 3.53 x 10(-6) +/- 0.872 x 10(-6) cm

28 crogram (mg wet weight of slice)-1 (mean +/- S.E.M.) at 1 week to 0.563 +/- 0.06 at 3 weeks of age (P

29 by (1.47 +/- 0.25) x 10(-6) cm s-1 (mean +/- S.E.M.).

30 ction it was 310 +/- 10 microM s-1 (mean +/- S.E.M., n = 11).

31 conditions was 6 +/- 1 microM s-1 (mean +/- S.E.M., n = 8 fibres); during isometric contraction it w

32 elocity of 3.8 +/- 0.70 mm min(-1) (mean +/- S.E.M. of 5 experiments).

33 stimated to be 1.9 +/- 0.3 m s(-1) (mean +/- S.E.M.).

34 e movement (Q(max)) (nC microF(-1), mean +/- S.E.M.) for S- and AS-CREB was 70.3 +/- 2.9 and 52.8 +/-

35 rol fibres (1.91 +/- 0.048 m s(-1), mean +/- S.E.M., n = 32 fibres) agreed with earlier values report

36 etoprolol (0.16 +/- 0.01 mg kg(-1); mean +/- S.E.M.) or glycopyrrolate (12.6 +/- 1.6 microg kg-1).

37 equency (0.4 +/- 0.22 impulses s-1, mean +/- S.E.M.) in the twenty-two units sensitive to such energy

38 gamma was 0.9 +/- 0.1 nC microF-1. (mean +/- S.E.M., n = 18).

39 ection by -49.6 +/- 4.0 mV (n = 12; mean +/- S.E.M.), without appreciable effects on membrane conduct

40 delta Vm = 53.2 +/- 7.0 mV; n = 13; mean +/- S.E.M.) than naive NCX (delta Vm = 10.6 +/- 2.0; n = 8)

41 fura-2 transient to 10.9 +/- 4.19% (mean +/- S.E.M., n = 7; equivalent to 6.5% of the Ca2+ transient)

42 ing rate (5.00 +/- 0.88 spikes s-1; mean +/- S.E.M., n = 55) of the responsive cells was significantl

43 ve cells (2.65 +/- 0.33 spikes s-1; mean +/- S.E.M., n = 74; P < 0.01; Student's unpaired t test).

44 lder (n = 9, 64 +/- 2 years, 8M/1F, mean +/- S.E.M.) versus young (n = 9, 26 +/- 1 years, 8M/1F) heal

45 perventilation induced by 7% CO(2) (mean +/- S.E.M., 135 +/- 10 ml (100 g)(-1) min(-1)) compared with

46 nous HA mass, 181+/-8 microg (n=26, mean +/- S.E.M.), and basal secretion rate, 4.4+/-0.4 microg h(-1

47 (8.63 +/- 0.92 vs. 16.17 +/- 1.37; Mean +/- S.E.M.).

48 an early rise in CBF (15.0 +/- 4%, mean +/- S.E.M., P < 0.05) by 10 min which remained elevated for

49 reased by a factor of 5.23 +/- 1.5 (mean +/- S.E.M.) over the conductance at low pressures (just abov

50 fura-2 transient of 12.2 +/- 1.5% (mean +/- S.E.M., n = 7; equivalent to a 22% increase in the Ca2+

51 r phase was increased by 34 +/- 6% (mean +/- S.E.M., n = 21) when compared with unconditioned transie

52 ivity increased from 3.08 +/- 0.68 (mean +/- S.E.M.) to 8.36 +/- 1.8 ng ml-1 hr-1.

53 (71.2 +/- 5.94 vs. 29.40 +/- 8.87; Mean +/- S.E.M., sec.), were also significantly reduced by a sing

54 had haematocrits of 55.0 +/- 0.9% (mean +/- S.E.M.) and 41.9 +/- 0.5%, respectively.

55 n ten of these vessels, which had a mean +/- S.E.M. Pb of 84.2 +/- 6.5 cmH2O, microvascular pressure

56 ed in twenty-nine vessels and had a mean +/- S.E.M. value of 79.6 +/- 5.0 cmH2O.

57 uli (7.4 +/- 0.5 events per animal, mean +/- S.E.M., n = 5, P = 0.002).

58 nules of tissues at 12-20 The P(B) (mean +/- S.E.M.) in 22 vessels between 12 and 20 degrees C, P(B)

59 baseline (35 +/- 5% above baseline, mean +/- S.E.M., P < 0.05) in the high-intensity group but not in

60 The viscosity coefficient (mean +/- S.E.M., 2 +/- 0.01 kN s m-2, n = 12) and the relaxation

61 ient to 64.01 +/- 2.09% of control (mean +/- S.E.M., n = 19 cells).

62 Ca,L to 10.25 +/- 2.25% of control (mean +/- S.E.M., n = 7 cells).

63 icroM; day 2 of exposure) controls (mean +/- S.E.M. maximum peak inward current density of -8.23 +/-

64 had a slow activation time course (mean +/- S.E.M. 10-90 % rise time 12.5 +/- 1.6 ms; n = 9 patches)

65 (938 +/- 152 versus 182 +/- 57 CSI; mean +/- S.E.M., P < 0.001).

66 severity, afterdischarge duration (Mean +/- S.E.M., sec.) (stimulated amygdala [87.40 +/- 5.47 vs. 5

67 hy subjects (five male, one female; mean +/- S.E.M. age = 31.7+/-1.6 years, normoxic maximal VO2 (VO2

68 8.3 +/- 1.3 microM Pi/mg protein/h (mean +/- S.E.M.).

69 y women: 73 postmenopausal (41 HRT, mean +/- S.E.M. 61 +/- 1 years; 32 no-HRT, 63 +/- 2 years) and 30

70 ns were: group 1, 0.91 +/- 0.12 Hz (mean +/- S.E.M., n = 5); group 2, 0.81 +/- 0.04 Hz (n = 18); grou

71 tration rates (0.2 g l-1 infusates; mean +/- S.E.M.), 1.60 +/- 0.09 times at intermediate filtration

72 caused a 41.6 +/- 4.7% inhibition (mean +/- S.E.M.; n = 7) of pinacidil-evoked whole-cell KATP curre

73 ning of 1 % L0, ATP was 21 +/- 1 M (mean +/- S.E.M., n = 3).

74 of 0.639 +/- 0.106 pmol/150 microl (mean +/- S.E.M.; n = 12).

75 peak amplitude, 9.4 +/- 1.0 microM (mean +/- S.E.M.); half-duration, 7.7 +/- 0.6 ms; fast-twitch: pea

76 1 microM, and 73+/-5% at 5 microM (mean +/- S.E.M., n = 10, P<0.05 for each dose vs. control).

77 ith an IC50 of 17.0 +/- 1.2 microM (mean +/- S.E.M., n = 4).

78 th an IC50 of 32.8 +/- 0.52 microM (mean +/- S.E.M., n = 5).

79 th an IC50 of 10.0 +/- 0.76 microM (mean +/- S.E.M., n = 5).

80 velocity, and was 84 +/- 9 microM (mean +/- S.E.M., n = 6) for shortening of 10 % L0.

81 [Ca2+]50) was 1.09 +/- 0.02 microM (mean +/- S.E.M., n = 61 contractions).

82 ine diameter of 96 +/- 18.3 microm, mean +/- S.E.M.) and venules (-14.4 +/- 4.0% from 249 +/- 25.8 mi

83 at both high- (EC50, 35+/-9 microM, mean +/- S.E.M., n = 3) and low- (EC50 >2 mM) affinity sites.

84 single site (EC50, 60+/-14 microM, mean +/- S.E.M., n = 3) or that it acts at both high- (EC50, 35+/

85 constant 43.3 +/- 2.0 microseconds, mean +/- S.E.M., n = 9) was similar between motor and sensory fib

86 7.35 was attained 30.4 +/- 2.7 min (mean +/- S.E.M.) after the end of exercise in the IPE protocol an

87 following OGD from 7.6 +/- 0.6 min (mean +/- S.E.M., n = 16) to 17.4 +/- 2.6 min (n = 6; p < 0.01).

88 culum (SR) Ca2+ was 2.9 +/- 0.4 mM (mean +/- S.E.M., n = 10).

89 Total [Mg2+]i was 1.29 +/- 0.08 mM (mean +/- S.E.M., n = 5), similar to that reported in the literatu

90 ygenated cells to 0.52 +/- 0.04 mM (mean +/- S.E.M., n = 5; P < 0.05) in deoxygenated ones.

91 l of the calf by 47.4 +/- 2.4 mmHg (mean +/- S.E.M.).

92 imal stimulation was 56 +/- 1 mmHg (mean +/- S.E.M., 3 sheep) for the O2-dependent component of K+ in

93 2 decreased from 40.0 +/- 4.8 mmHg (mean +/- S.E.M., n = 6) at the base to 30.4 +/- 5.2 mmHg (n = 6)

94 arterial pressure by 17 +/- 2 mmHg (mean +/- S.E.M.; P < 0.001) and also had a significant negative c

95 d an amplitude of 3.00 +/- 0.19 mV (mean +/- S.E.M.) and lasted for 1.02 +/- 0.06 s.

96 imum amplitudes of 12.2 +/- 0.7 mV (mean +/- S.E.M.) around -70 mV.

97 e membrane potential (7 +/- 0.7 mV; mean +/- S.E.M.; n = 105) and decreased the input resistance in 8

98 membrane potential (10 +/- 0.8 mV; mean +/- S.E.M.; n = 27) or produced an inward current of 1.6 +/-

99 there were 15,135 +/- 356 neurons (mean +/- S.E.M.) in the FVB/N strain, and 10,645 +/- 315 neurons

100 hronic paroxetine (22.2 +/- 1.4 nM, mean +/- S.E.M.) than water (15.8 +/- 1.4 nM).

101 /- 0.9 microl min(-1) at 3 cmH(2)O, mean +/- S.E.M.; n = 6).

102 pulses, had a peak of 17 +/- 1 pA (mean +/- S.E.M.) and lasted for 2.8 +/- 0.1 s.

103 d by a single AP was 39 +/- 2.8 pC (mean +/- S.E.M.) and did not change significantly during trains o

104 .7 and 39.8 +/- 7.0%, respectively (mean +/- S.E.M., n = 6).

105 Phase shifts (mean +/- S.E.M., h) in muscimol/8-OH-DPAT-microinjected hamsters

106 The mean +/- S.E.M. control arterial blood flow at the lowest venous

107 protocols and than before training (mean +/- S.E.M. reduction in end-tidal PCO2 = 1.32 +/- 0.36 Torr,

108 ccurred in 0.12 +/- 0.01 pCa units (mean +/- S.E.M., n = 61) for a SL of 2.2 micron and 0.17 +/- 0.01

109 2 +/- 6 % of MEP with no vibration; mean +/- S.E.M.), but suppressed MEPs in the two non-vibrated han

110 equencies (54 +/- 5 vs. 56 +/- 5 W; mean +/- S.E.M.).

111 omprised 73 +/- 3% water by weight (mean +/- S.E.M.).

112 in seven subjects (25 +/- 1 years, mean +/- S.E.M.) using the variable-pressure neck collar techniqu

113 Seven young (28 +/- 2 years; mean +/- S.E.M.) and eight older (64 +/- 2 years) healthy, normot

114 the experiment, reaching 8.0+/-0.5% (mean+/-S.E.M.) above pre-injection control values 165 min after

115 bition for static (2.4+/-0.2 ms, n=6; mean+/-S.E.M.) and dynamic (2.2+/-0.2 ms, n=7) gamma-motoneuron

116 nical stimuli (from 4+/-2 to 41+/-7%; mean+/-S.E.M.) and a decrease in withdrawal latency to heat (fr

117 The coronal infarct area (mean+/-S.E.M.) was 19.3+/-1.8% for vehicle treated rats vs. 8.0

118 The coronal infarct area (mean+/-S.E.M.) was 9.5+/-1.0% for intact female rats, 16.6+/-1.

119 n consciously free-moving mice (Delta mean+/-S.E.M.=-12.3+/-3.2 mm Hg for moxonidine versus -13.5+/-1

120 , striatum and hemisphere (hemisphere mean+/-S.E.M. : 41.2+/-5.4 vs. 82.4+/-9.2 microg/g, p=0.005) co

121 ic rabbit brain was 3.5+/-0.3 mm/min (mean+/-S.E.M., n=14).

122 in noncholinergic multipolar neurons (mean+/-S.E.M.; 355.7+/-15.4 microm2) located primarily outside

123 nels with a conductance of 55+/-4 pS (mean+/-S.E.M.; n=3), were observed in cell-attached patches.

124 e two genotypes prior to stimulation (mean+/-S.E.M.=3.8+/-0.5 fmol/microl, lean; 3.6+/-1.0 fmol/micro

125 .6+/-4.7 min in NGF-infused subjects (mean+/-S.E.M.).

126 -0.0094 cm(3)/min/g wet brain weight, mean+/-S.E.M., n=four rats) was significantly decreased by 1000

127 st-hypoxia; MK-801, -0.5 +/- 4.1%, means +/- S.E.M.), with little change in both the CO2-apnoeic thre

128 ypoxia (56 +/- 14 and 73 +/- 16 % (means +/- S.E.M.) at 60 min post-hypoxia, respectively; both P < 0

129 l coefficient, nH = 1.53 +/- 0.36 (means +/- S.E.M.).

130 /- 7.3 to 170 +/- 9.8 beats min-4 (means +/- S.E.M.) for 3-4 min, first during an infusion of the sol

131 0.16 pC, z = 0.88 +/- 0.02; n = 5, means +/- S.E.M.).

132 - 1.0; final control, 6.2 +/- 0.7 (means +/- S.E.M.; n = 21, P < 0.025).

133 enated cells (by 4 +/- 1-fold; all means +/- S.E.M., n = 3).

134 ons in iliac vascular conductance (means +/- S.E.M.) were 45 +/- 6 %, 30 +/- 4 %, 26 +/- 3 % and 17 +

135 Baseline supine values were: MAP (means +/- S.E.M.) 84.9 +/- 3.2 mmHg; HR, 63.9 +/- 3.2 beats min-1;

136 : 37 +/- 5.6 and 1.41 +/- 0.15 ms, means +/- S.E.M.).

137 tively, in perinatal-treated rats (means +/- S.E.M.), but increased more in untreated control rats (5

138 s and 1.7 +/- 0.4 s, respectively (means +/- S.E.M.).

139 /- 0.10 versus 0.45 +/- 0.05 pN s, means +/- S.E.M., P = 0.01).

140 x mm(-2) respectively (all values means +/- S.E.M., n = 6 for UCP-3tg and n = 5 for wild-type).

141 NAME conditions for baseline .VO2 (means +/- S.E.M. 797 +/- 32 vs. 794 +/- 29), the duration of phase

142 A/deltat = 4.2 +/- 0.7 microM s(-1) (means+/-S.E.M., n=15).

143 , 16+/-3% and 11+/-3%, respectively, means+/-S.E.M.).

144 mplitude of NRGc-evoked IPSPs (1.9+/-0.2 mV (S.E.M.) vs. 1.4+/-0.2 mV; n=11, control and naloxone, re

145 n B3 neurons after OC stimulation (-89.0 mV, S.E.M.=14.1, n=10) and the octopamine response of the B3

146 pamine response of the B3 neurons (-84.7 mV, S.E.M.=6.6, n=6) indicate that increased K(+)-conductanc

147 arts (expressed in microl per mg protein +/- S.E.M., n = 6), determined with (3)H(2)O and [(14)C]sucr

148 eurons (1.44 +/- 0.60 neurons/reticle; x +/- S.E.M.) compared to sham rats (58.57 +/- 0.69).