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3 13.6 +/- 1.4 units/mg of protein (n = 22, +/-S.E.), whereas the A334T mutation yielded an enzyme with
5 Km for ATP of 680 +/- 226 microM (n = 3, +/-S.E.), the Michaelis constant for (RS)-mevalonate was in
7 he mean difference in signal ratios of 0.47 (S.E. 0.012, adjusted for clustering of observations with
10 0.26 +/- 0.02 unit/mg of protein (n = 6, +/-S.E.), representing a decrease to 1.4% of control Vmax.
11 decreased LKB1 kinase activity by 31 +/- 9% (S.E.) but had no effect on the association of LKB1 with
14 search Institute for Scientists Emeriti (R.I.S.E.) at Drew University have been very rewarding and ar
16 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
17 trans- Golgi pH was 6.25 +/- 0.04 (mean +/- S.E.; n = 80, vector control), 6.30 +/- 0.03 (n = 74, CF
18 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
25 or one line and 88.8 +/- 1.6 mm Hg (mean +/- S.E., n = 19, P < 0.001) for another, as compared with 1
26 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
27 150 +/- 23 and 440 +/- 190 microM (mean +/- S.E.) for substrates (RS)-mevalonate and ATP, respective
28 l thickness in vivo was (in microm, mean +/- S.E., n = 5 mice) 123 +/- 1 (wild type), 101 +/- 2 (AQP1
38 baseline diameter=94+/-5 micrometers, mean+/-S.E.) were measured using a closed cranial window in ane
42 by 30, or 60 min of reperfusion, the Mean+/-S.E. (n=5) percentage of maximal cTnI release was 30 +/-
43 ation was rapid (t((1)/(2)), 7.3 +/- 0.4 ms, S.E., n = 11 mice) and blocked by acetazolamide and incr
47 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
49 ontained (in units of mmol/kg dry weight +/- S.E.) large amounts of phosphorus (1390 +/- 13), magnesi
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