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3 n average tHb of the Tis-T1 group were 102.0 micromol/L +/- 28.5 (standard deviation) and 71.9 microm
4 a linear response range from 5.0 up to 200.0 micromol L(-1), detection limit of 8.25 nmol L(-1) and a
5 nsor has a linear response in the 0.05-250.0 micromol L(-1) concentration range, a very good detectio
10 fter 24 h of high light (approximately 1,000 micromol m(-2) s(-1)), as shown by the decline in maximu
11 centration values ranging from 100 to 10,000 micromol/mol with relative expanded uncertainties (95% c
12 ol/L; in whole brain, they are 10,000-12,000 micromol/L but only 0.5-2 micromol/L in extracellular fl
13 linder gas mixtures: set no. 1, He at 12,000 micromol/mol, H(2) at 600 micromol/mol, Ar at 100 microm
14 at 600 micromol/mol; set no. 2, He at 15 000 micromol/mol, H(2) at 5000 micromol/mol, Ar at 1000 micr
15 (1,200 micromol mol(-1)) and SE CO(2) (4,000 micromol mol(-1)), at two developmental stages early and
16 xide-supported catalyst, yield around 22,000 micromoles of acetic acid per gram of catalyst, or aroun
17 urinary sodium excretion (from 0.07 +/- 0.01 micromol min(-1) at baseline to 0.76 +/- 0.08 micromol m
18 as also markedly increased (0.22 versus 0.01 micromol/L) in the UDCA group compared to the placebo gr
19 de concentration (mean +/- SD: 0.52 +/- 0.02 micromol/250 g) in the meat of the SBs compared with the
22 +/- 0.05 vs. 0.25 +/- 0.07 vs. 0.32 +/- 0.05 micromol kg adipose lipid(-1) min(-1), respectively (P =
23 +/- 0.06 vs. 0.20 +/- 0.05 vs. 0.31 +/- 0.05 micromol kg adipose lipid(-1) min(-1), respectively (P =
24 changes in the UDCA level (16.86 versus 0.05 micromol/L) and total bile acid level (17.21 versus -0.5
25 was higher (0.12 +/- 0.05 vs. 0.03 +/- 0.06 micromol x g(-1) x h(-1), means +/- SD, P < 0.02, n = 5)
26 an: 0.70 micromol/L, IQR: 0.40-0.84 vs. 0.06 micromol/L; IQR: 0.01-.018; p = 0.002), cobalt (median:
27 centrations had increased from 1.78 +/- 0.07 micromol/L at baseline to 2.85 +/- 0.11 micromol/L for m
28 og/L (3.65 nmol/L) and 1.58 microg/dL (0.076 micromol/L), respectively, in 14,778 adults aged >or=20
31 ndependent of antifibrotic actions, RLX (0.1 micromol/L) increased Na(+) current density, INa ( appro
32 tion of CaV1.2 channels with nifedipine (0.1 micromol/L) or diltiazem (10 micromol/L) abolished this
34 10 micromol/L), PD98059 (MEK1 inhibitor, 0.1 micromol/L), and wortmannin (phosphatidylinositol 3-kina
36 te autonomic stimulation (acetylcholine [0.1 micromol/L] or isoproterenol [0.01-0.1 micromol/L]) afte
37 [0.1 micromol/L] or isoproterenol [0.01-0.1 micromol/L]) after termination of atrial tachypacing (5-
38 2, 0.9 +/- 2.1, 8.6 +/- 2.3, and 6.0 +/- 1.1 micromol kg(-1) min(-1) within 5 h in control, LY0.25, L
39 rol subjects (PCr=5.4+/-1.2 versus 9.6+/-1.1 micromol/g wet weight in MI versus control subjects, res
40 lasma (6.9 +/- 1.9 compared with 6.7 +/- 1.1 micromol/L) or RBCs (2068 +/- 50 compared with 2117 +/-
41 tration decreased (from 35 +/- 2 to 14 +/- 1 micromol/L) and the grand median [quartiles] FGF21 conce
42 QR: 111-145; p<0.001) and zinc (median: 23.1 micromol/L, IQR: 12.9-32.6 vs. 5.1 micromol/L; IQR: 4.4-
43 : 0.01-.018; p = 0.002), cobalt (median: 3.1 micromol/L, IQR: 2.62-3.15 vs. 1.17 micromol/L; IQR: 0.9
44 xygen consumption (from 59 +/- 5 to 34 +/- 1 micromol oxygen/min/10(6) cells, P < 0.001); the latter
46 ian: 23.1 micromol/L, IQR: 12.9-32.6 vs. 5.1 micromol/L; IQR: 4.4-9.4; p = 0.020) when compared with
47 an average tHb of the benign group were 55.1 micromol/L +/- 22.7 and 39.1 micromol/L +/- 14.9, respec
48 KBP12] in intact myocytes is approximately 1 micromol/L (similar to [RyR]), whereas [FKBP12.6] is <or
50 ent with the parent compound (I3C) or DIM (1 micromol/L) protected against cell killing due to H(2)O(
51 led that the Rho-kinase inhibitor fasudil (1 micromol/L) significantly blunted artery contractions to
56 nhibited CDK2 at concentrations lower than 1 micromol/L, with CDK2 being inhibited 35-fold less poten
57 ) cells with VEGF (10 ng/ml), ANP (1 pM to 1 micromol/L), and/or isatin, an ANP receptor antagonist.
61 ug was tested at five concentrations (0.1-10 micromol/L) for its effects on YFP expression, cell viab
63 cells at high (100 nmol/L, 1 mmol/L, and 10 micromol/L, respectively) but not at physiologically rel
64 ype 5 inhibitor and adenosine antagonist, 10 micromol/L) and phorbol myristate acetate (phorbol ester
65 ion, approximately 0.28 and approximately 10 micromol/L) at a late stage of entry, (2) induce Niemann
67 l/L) and especially P(2)Y(12) (Cangrelor, 10 micromol/L) blunted CXCL16-triggered platelet activation
69 phorbol myristate acetate (phorbol ester, 10 micromol/L), and inhibited by H-89 (protein kinase A inh
71 ',5'-cyclic monophosphate [cAMP] inducer, 10 micromol/L; >3-fold), potentiated by 3-isobutyl-1-methyl
72 ited by H-89 (protein kinase A inhibitor, 10 micromol/L), PD98059 (MEK1 inhibitor, 0.1 micromol/L), a
73 half maximal inhibitory concentration of <10 micromol/L, a selectivity index>20, and potent activity
74 C-reactive protein <2 mg/L, homocysteine <10 micromol/L, N-terminal pro-brain natriuretic peptide <10
76 thelin-1- (10 nmol/L), or phenylephrine- (10 micromol/L) induced hypertrophic cultured neonatal ventr
77 For microarrays, cells were exposed to 10 micromol/L of tamoxifen and genes with expression change
80 4) revealed that adenosine perfusion (10-100 micromol/L) produced more significant shortening of acti
81 lutamate concentrations in plasma are 50-100 micromol/L; in whole brain, they are 10,000-12,000 micro
83 mol/mol, H(2) at 600 micromol/mol, Ar at 100 micromol/mol, and O(2) at 600 micromol/mol; set no. 2, H
84 purinergic receptors P(2)Y(1) (MRS2179, 100 micromol/L) and especially P(2)Y(12) (Cangrelor, 10 micr
85 erm N2-fixation rates were higher, up to 100 micromol N m(-2)d(-1), and detected N2fixation at all si
86 l/mol, H(2) at 5000 micromol/mol, Ar at 1000 micromol/mol, O(2) at 5000 micromol/mol; and set no. 3,
88 median creatinine at 3 and 12 months was 107 micromol/L (range 72-222) and 121 micromol/L (range 63-1
89 0.07 micromol/L at baseline to 2.85 +/- 0.11 micromol/L for men and from 1.64 +/- 0.04 to 3.32 +/- 0.
90 t follow-up in the lifestyle arm (beta=-0.11 micromol/L per genetic risk scores risk allele; 95% conf
91 2 carriers; 11.53 micromol/l/h, versus 12.11 micromol/l/h, P = 0.036) and after adjustment for age an
92 with high homocysteine (above the median, 11 micromol/L) and that, in these participants, a causal Ba
93 y acid: 8.97 + or - 1.39 to 4.53 + or - 1.12 micromol/min; glucose: 1.31 + or - 0.52 to 6.86 + or - 1
96 bits a specific decarboxylase activity of 12 micromol pyruvate min(-)(1) mg(-)(1) protein using benzy
97 group of 104 patients with tHcy level of 12 micromol/L or greater revealed that those subjects with
100 median: 311 micromol/L, IQR: 289-329 vs. 129 micromol/L; IQR: 111-145; p<0.001) and zinc (median: 23.
102 dase enzymatic activity than controls (11.14 micromol/l/h versus 11.85 micromol/l/h, P = 0.011).
103 ing concentrations of L-ascorbic acid (-4.15 micromol/L; 95% CI: -0.49, -7.81 micromol/L; P = 0.03 re
104 -2.23) and elevated homocysteine levels (>15 micromol/L: OR = 2.24; 95% CI = 1.38-3.63) were independ
105 of daily oral doses of sulforaphane (50-150 micromol) for 18 wk, followed by 4 wk without treatment,
109 malondialdehyde concentration (1.79 +/- 0.17 micromol/250 g) in the meat of the control burgers (CBs)
110 ian: 3.1 micromol/L, IQR: 2.62-3.15 vs. 1.17 micromol/L; IQR: 0.95-1.27; p<0.001), iron (median: 311
111 eir NHGU was blunted (68 +/- 9 and 16 +/- 17 micromol.100 g liver(-)(1).min(-)(1), respectively).
113 The genetic score raised uric acid by 17 micromol/L (95% CI 15, 18) per SD increase and explained
114 d HHcy and elevated Hcy levels to 53 and 173 micromol/L in Cbs(+/+) and Cbs(-/+) mice fed an HM diet,
115 ents in the highest BLL quartile (mean, 0.19 micromol/L [3.95 microg/dL]) compared with 1.76% (CI, 1.
117 for samples containing approximately 0.1-0.2 micromol of (13)C,(15)N- or (2)H,(13)C,(15)N-labeled pro
118 lthy volunteers, local infusion of SMTC (0.2 micromol/min) reduced radial artery blood flow by 36.0+/
120 y reduced in patients with AMD (median: 16.2 micromol/L, IQR: 11.4-31.3 vs. 49.9 micromol/L; IQR: 32.
123 In contrast, N(G)-monomethyl-L-arginine (2 micromol/min) infusion reduced radial blood flow to a si
125 kinase inhibitors and Akt inhibitor SH-6 (20 micromol/L) further diminished CXCL16-induced platelet a
126 0.001) and arginine levels (mean: 68 +/- 20 micromol/l vs. 74 +/- 24 micromol/l, p < 0.001) than tho
127 es revealed a UDP EC(50) of approximately 20 micromol/L and an ATP IC(50) of approximately 5 micromol
129 when glucose infusion rates (GIRs) were ~20 micromol kg(-1) min(-1) in all groups, was higher in con
130 ficantly increased, and when treated with 20 micromol/L (-)-epigallocatechin gallate (green tea) was
132 400 micromol mol(-1)), elevated CO(2) (1,200 micromol mol(-1)) and SE CO(2) (4,000 micromol mol(-1)),
133 known that super-elevated (SE) CO(2) (>1,200 micromol mol(-1)) induces physiological responses differ
134 at of moderately elevated CO(2) (up to 1,200 micromol mol(-1)), but little is known about the molecul
136 ux of (13)NH3/(13)NH4(+), which exceeded 200 micromol g(-1) h(-1), was not commensurate with membrane
138 Blood lead levels (BLLs) less than 1.21 micromol/L (<25 microg/dL) among adults are considered a
139 nt total bile acid levels (34.99 versus 9.21 micromol/L, P < 0.08) in comparison with those who did n
140 micromol/hr-cm(2)) and low (0.33 + or - 0.22 micromol/hr-cm(2)) fluxes that coincide with therapeutic
143 tic acid per gram of catalyst, or around 230 micromoles of methanol per gram of catalyst, respectivel
145 ol/l) and lower in vegetarians (230, 224-236 micromol/l) and fish eaters (227, 221-233 micromol/l).
146 ls (mean: 68 +/- 20 micromol/l vs. 74 +/- 24 micromol/l, p < 0.001) than those without significantly
148 phosphate (P) was found to be highest (~0.24 micromoles per kilogram per year) in the vicinity of the
149 icromol/l) than in meat eaters (237, 231-242 micromol/l) and lower in vegetarians (230, 224-236 micro
150 were slightly higher in vegans (241, 234-247 micromol/l) than in meat eaters (237, 231-242 micromol/l
152 NOS inhibitor N(G)-monomethyl-L-arginine (25 micromol/min) also reduced basal coronary flow (by 22.3+
156 ibroblasts were exposed to various FFAs (250 micromol/l) in either 5 or 25 mmol/l (high) glucose for
157 m sample of 36 anonymous individuals was 277 micromol/L erythrocyte lysate/hour with a standard devia
159 8.8, and those of the T2-T4 group were 100.3 micromol/L +/- 26.4 and 67.0 micromol/L +/- 18.3, respec
161 ession with CsCl (5 mmol/L, n=3), BaCl(2) (3 micromol/L, n=3), and low extracellular potassium (1 mmo
162 yme A recycling, in nontransgenic (4.5+/-2.3 micromol/min per gram dry weight) was 3.75-fold faster t
164 eak concentrations of approximately 1 to > 3 micromol/L could also be monitored in blood vessels of t
166 /AFL induced by acetylcholine (ACh; 0.3 to 3 micromol/L) and/or isoproterenol (Iso; 0.2 to 1 micromol
167 [quartiles 30.8, 61.8] vs. 51.9 [41.0, 77.3] micromol glucose/microU insulin . mL(-1) . min(-1); P <
169 concentrations of BCAA ranging from 8 to 30 micromol/liter, which is 10 to 17% of the concentration
171 IQR: 0.95-1.27; p<0.001), iron (median: 311 micromol/L, IQR: 289-329 vs. 129 micromol/L; IQR: 111-14
173 6-324 micromol/l), fish eaters (309, 300-318 micromol/l) and vegetarians (303, 294-312 micromol/l).
174 ol/l), followed by meat eaters (315, 306-324 micromol/l), fish eaters (309, 300-318 micromol/l) and v
176 paclobutrazol (PAC) at ambient [CO(2)] (350 micromol CO(2) mol(-1)) was reverted by elevated [CO(2)]
177 ration (340, 95% confidence interval 329-351 micromol/l), followed by meat eaters (315, 306-324 micro
179 [K(+)]ext and yielding fluxes as high as 36 micromol g (root fresh weight)(-1) h(-1) at 5 mm [K(+)]e
185 ssociated with blood GSH (mean change, -25.4 micromol/L; 95% CI: -45.3, -5.31) and plasma CySS (mean
187 R, 1.35 [CI, 1.14 to 1.60] per 1 mg/dL [88.4 micromol/L]), and lower triage systolic blood pressure (
189 in patients with isolated endarteritis, 96.4 micromol/L (95% CI, 48.6 to 143.2) in positive controls
190 nd during perfusion of either chloroquine (4 micromol/L, n=7) or flecainide (2-4 micromol/L, n=5).
191 e grown under ambient atmospheric CO(2) (400 micromol mol(-1)), elevated CO(2) (1,200 micromol mol(-1
192 30) were grown and monitored at ambient (400 micromol mol(-1)) or elevated (800 micromol mol(-1)) [CO
193 methylarginine concentration in plasma (1.41 micromol/L in the endo-DDAH1(-/-) versus 0.69 micromol/L
195 calculated from microsensor profiles (31-437 micromol CH4m(-2)d(-1)) were sufficiently high to preven
196 creatinine greater than 25% or 0.5 mg/dL (44 micromol/L) from baseline to peak value within the first
199 e unconfounded effect, we found that a 59.48 micromol/L higher uric acid concentration did not have a
202 was blocked in rat hearts perfused with 2.5 micromol/L TAT-HK2 before ischemia or at the onset of re
203 lux were suppressed to 23 +/- 3 and 26 +/- 5 micromol L(-1) (P = 0.91) and 44 +/- 4 and 39 +/- 5 micr
204 l L(-1) (P = 0.91) and 44 +/- 4 and 39 +/- 5 micromol min(-1) (P = 0.41) in the insulin and niacin gr
207 a selective AMPK inhibitor (compound C, at 5 micromol/L) reversed the effects of metformin on [Ca(2+)
210 xylic acids have the potential to supply 4-5 micromoles C hr(-1)g(-1) fresh weight to the soil soluti
212 At 48 hours, cells exposed to 10 and 50 micromol/L of tamoxifen were 85.6% and 48.4% viable, res
213 t 5000 micromol/mol; and set no. 3, He at 50 micromol/mol, H(2), Ar, and O(2) each at 25 micromol/mol
215 rothrombin time <50% and serum bilirubin >50 micromol/L on postoperative day 5) and the International
216 sulfide-donor sodium hydrosulfide (NaHS) (50 micromol/kg, twice daily) or vehicle (n=7 per group).
221 . 2, He at 15 000 micromol/mol, H(2) at 5000 micromol/mol, Ar at 1000 micromol/mol, O(2) at 5000 micr
222 l/mol, Ar at 1000 micromol/mol, O(2) at 5000 micromol/mol; and set no. 3, He at 50 micromol/mol, H(2)
223 clusion of all GBA and LRRK2 carriers; 11.53 micromol/l/h, versus 12.11 micromol/l/h, P = 0.036) and
224 nd total bile acid level (17.21 versus -0.55 micromol/L) were significantly higher in the UDCA group
225 the ranges of 0.01-250, 1.0-500, and 3.0-550 micromol L(-)(1), with detection limits of 0.007, 0.6, a
226 Growth of soybean at elevated [CO(2)] (550 micromol x mol(-1)) under field conditions stimulated th
227 ations in the range of 0.004-340 and 0.5-550 micromol L(-1), with detection limits of 1.0 nmol L(-1)
230 betic CTGF+/+ group (11.7+/-1.2 vs 7.9+/-0.6 micromol/L p<0.01), while urinary albumin excretion and
231 1 month after rejection treatment was 132.6 micromol/L (95% confidence interval [95% CI], 78.7 to 18
232 3.2) in positive controls (P=0.32), and 18.6 micromol/L (95% CI, 1.8 to 35.4) in untreated negative c
234 our different levels (100, 200, 400, and 600 micromol m(-2) s(-1)) by imaging chlorophyll fluorescenc
235 o. 1, He at 12,000 micromol/mol, H(2) at 600 micromol/mol, Ar at 100 micromol/mol, and O(2) at 600 mi
236 mol, Ar at 100 micromol/mol, and O(2) at 600 micromol/mol; set no. 2, He at 15 000 micromol/mol, H(2)
240 eries, intracoronary infusion of SMTC (0.625 micromol/min) reduced basal coronary blood flow by 34.1+
241 99.0+/-40.1 mg.dL(-1)) and Lp(a) 3.74+/-1.63 micromol.L(-1) (104.9+/-45.7 mg.dL(-1)), respectively.
242 e amniotic fluid embolism group (234 134-635 micromol/L) compared with the non-amniotic fluid embolis
243 between the soil surface and the leaves (638 micromol mol(-1)) and the atmosphere at 20 cm above grou
244 ssfully switch between high (1.3 + or - 0.65 micromol/hr-cm(2)) and low (0.33 + or - 0.22 micromol/hr
246 icromol/L in the endo-DDAH1(-/-) versus 0.69 micromol/L in the control mice), kidney, lung, and liver
249 ive breast cancer in mice at a low dose (1.7 micromol kg(-1), 1 T), but not in oestrogen receptor-pos
251 U/L), and serum bilirubin (mean peak, 160.7 micromol/L [9.4 mg/dL]; range, 34.2 to 356 micromol/L [2
252 ansplantation, high serum creatinine (>291.7 micromol/L), or retinal photocoagulation or vitrectomy (
253 queous humor levels of cadmium (median: 0.70 micromol/L, IQR: 0.40-0.84 vs. 0.06 micromol/L; IQR: 0.0
254 ions for C-mannosyltryptophan were 0.26/0.72 micromol/L and 3.39/4.30 micromol/mmol creatinine, respe
260 (79 micromol/L [IQR, 70-87 micromol/L] vs 79 micromol/L [IQR, 72-89 micromol/L], P = .61) and glycate
262 rs, serum iron had increased by 15.9 +/- 9.8 micromol/L from baseline in lexaptepid-treated subjects
263 ient (400 micromol mol(-1)) or elevated (800 micromol mol(-1)) [CO2] for 120 d and subjected to droug
265 ymatic activity than GBA heterozygotes (0.85 micromol/l/h versus 7.88 micromol/l/h, P < 0.001), and G
266 Zinc concentrations were approximately -1.85 micromol/L lower in depressed subjects than control subj
268 ine concentration (79 micromol/L [IQR, 70-87 micromol/L] vs 79 micromol/L [IQR, 72-89 micromol/L], P
269 tivity than GBA and LRRK2 non-carriers (7.88 micromol/l/h versus 11.93 micromol/l/h, P < 0.001).
270 heterozygotes (0.85 micromol/l/h versus 7.88 micromol/l/h, P < 0.001), and GBA heterozygotes had lowe
273 -87 micromol/L] vs 79 micromol/L [IQR, 72-89 micromol/L], P = .61) and glycated hemoglobin (5.9% [IQR
274 es calculated from cell densities (660-4,890 micromol CH4m(-2)d(-1)) and actual rates calculated from
278 an: 16.2 micromol/L, IQR: 11.4-31.3 vs. 49.9 micromol/L; IQR: 32.0-.142.0; p = 0.022) when compared t
279 mol/L +/- 28.5 (standard deviation) and 71.9 micromol/L +/- 18.8, and those of the T2-T4 group were 1
281 r groups, which had serum levels of 56 36-91 micromol/L, 65 39-91 micromol/L and 49 30-78 micromol/L,
282 erum levels of 56 36-91 micromol/L, 65 39-91 micromol/L and 49 30-78 micromol/L, respectively (p < .0
285 participants), fibrinogen by 10% (mean -0.96 micromol/l, three trials, 159 participants), ADP platele
286 g concentrations of L-ascorbic acid of -5.98 micromol/L (95% CI: -8.23, -3.73 micromol/L; P = 2.0 x 1
287 ols (median L-arginine level, 65, 66, and 98 micromol/mL, respectively [P = .0001]; median L-arginine
288 y (reciprocal of glucose rate of appearance [micromol x kg fat-free mass(-1) x min(-1)] x insulin [mU
289 sure brain glucose metabolism (quantified as micromol/100 g/min), which serves as a marker of brain f
291 Urinary malondialdehyde concentrations (micromol/g creatinine) decreased by 49% (P = 0.021) in s
293 Hepatic glucose and intermediate fluxes (micromol . kg(-1) . min(-1)) were measured with and with
296 ery good detection sensitivity (0.4177 muA L micromol(-1)), and a low detection limit of 1x10(-2) mum
298 MMA concentration expressed as the ratio of micromoles of MMA to millimoles of creatinine (uMMA rati
302 4 (192.0) ng/mL, respectively (to convert to micromoles per liter, multiply by 0.00489; P = .07).
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