ライフサイエンスコーパス: mmol

1 trations were 2.35 mmol/L (91 mg/dL) and 1.0 mmol/L (39.5 mg/dL), respectively; obesity, hypertension

2 or 150 to 180 mg per deciliter (8.3 to 10.0 mmol per liter; higher-target group).

3 rget glucose concentration range of 5.6-10.0 mmol/L during the 72 h study period.

4 the glucose range of 70-180 mg/dL (3.9-10.0 mmol/L) is improved by initiation of CSII in adults with

5 concentration was in target range (3.9-10.0 mmol/L) over the 4 week study period.

6 oncentration range of 70-180 mg/dL (3.9-10.0 mmol/L) was 791 min per day (SD 157) in the CGM plus CSI

7 oncentration range of 70-180 mg/dL (3.9-10.0 mmol/L).

8 the area under the curve for 180 mg/dL [10.0 mmol/L]), but also an increase in CGM-measured hypoglyca

9 four metrics: p=0.007 for >180 mg/dL [>10.0 mmol/L], p=0.02 for >250 mg/dL [>13.9 mmol/L], p=0.04 fo

10 HO 2 h glucose concentration cutoff 7.8-11.0 mmol/L).

11 levels reached a nadir of approximately 2.0 mmol/L, and epinephrine rose to approximately 900 pg/mL.

12 f C-DBP precursors decreased from 6.8 to 3.0 mmol/mol-C at initial-exponential phase then increased t

13 calibration curves in the range of 0.10-5.0 mmol L(-1).

14 ined during hyperinsulinemic-euglycemic (5.0 mmol/L)-hypoglycemic (2.6 mmol/L) clamps in 11 healthy p

15 olesterol level was 3.6 mmol/L (normal, <5.0 mmol/L).

16 framework materials at 298 K and 1 bar (6.0 mmol g(-1)) and involves hydrogen bonding between the OH

17 Glucose was maintained at euglycemia (6.0 mmol/L) or hypoglycemia (2.5 mmol/L) for 1 h.

18 (HbA1c between >/=7.7% and </=11.0% [>/=61.0 mmol/mol and </=97.0 mmol/mol]) and had been prescribed

19 s elevated levels of fasting glucose (>/=7.0 mmol/L [>/=126 mg/dL]) and hemoglobin A1c (>/=6.5%) in p

20 ization (WHO) criteria to define GDM: >/=7.0 mmol/L for fasting glucose and/or >/=7.8 mmol/L for 2-h

21 eater or fasting plasma glucose (FPG) of 7.0 mmol/L or greater.

22 FPG 5.6-6.9 mmol/L), or diabetic (FPG >/=7.0 mmol/L).

23 .6) in the bionic pancreas period versus 9.0 mmol/L (1.6) in the comparator period (difference 1.1 mm

24 % and </=11.0% [>/=61.0 mmol/mol and </=97.0 mmol/mol]) and had been prescribed insulin for at least

25 ranges (before/after change +0.07 +/- 0.006 mmol/L), and total-to-ionized calcium ratio, a surrogate

26 on compared to those without (+0.2 vs -0.006 mmol/L/hr; p < 0.001).

27 me [weighted mean difference (95% CI): -0.01 mmol/L (-0.08, 0.06 mmol/L), 0.02 mmol/L (-0.05, 0.08 mm

28 Exceptionally high SO2 capacity of 11.01 mmol g(-1) is achieved at atmosphere pressure by SIFSIX-

29 CI): -0.01 mmol/L (-0.08, 0.06 mmol/L), 0.02 mmol/L (-0.05, 0.08 mmol/L), 0.03 mmol/L (-0.01, 0.07 mm

30 ycerides (-0.08 mmol/L; 95% CI: -0.14, -0.02 mmol/L), and body weight (-1.40 kg; 95% CI: -2.07, -0.74

31 hode was 0.153 +/- 0.010 and 0.586 +/- 0.029 mmol CH4/mg biomass-day, respectively.

32 l/L), 0.02 mmol/L (-0.05, 0.08 mmol/L), 0.03 mmol/L (-0.01, 0.07 mmol/L), and 0.04 mmol/L (-0.02, 0.1

33 olesterol level of 40 mg per deciliter (1.03 mmol per liter).

34 glucose (-0.14 mmol/L; 95% CI: -0.24, -0.036 mmol/L), HbA1c [-10 g/L (95% CI: -12.90, -7.10 g/L; impa

35 , 0.03 mmol/L (-0.01, 0.07 mmol/L), and 0.04 mmol/L (-0.02, 0.10 mmol/L); -0.08 mm Hg (-0.26, 0.11 mm

36 althy controls and patients with cALD (0.042 mmol trolox equivalent; P < .01).

37 fference (95% CI): -0.01 mmol/L (-0.08, 0.06 mmol/L), 0.02 mmol/L (-0.05, 0.08 mmol/L), 0.03 mmol/L (

38 0.05, 0.08 mmol/L), 0.03 mmol/L (-0.01, 0.07 mmol/L), and 0.04 mmol/L (-0.02, 0.10 mmol/L); -0.08 mm

39 dministrations (mean accumulated dose, 32.07 mmol +/- 17.62, with an average of 16.7 weeks +/- 7.9 be

40 0.08, 0.06 mmol/L), 0.02 mmol/L (-0.05, 0.08 mmol/L), 0.03 mmol/L (-0.01, 0.07 mmol/L), and 0.04 mmol

41 3 g/L; normoglycemia)], triglycerides (-0.08 mmol/L; 95% CI: -0.14, -0.02 mmol/L), and body weight (-

42 iations with increased fasting glucose (0.09 mmol/L, 95% CI 0.02 to 0.15), bodyweight (1.03 kg, 0.24

43 sors in the control ranged from 2.41 to 3.09 mmol/mol-C.

44 ions of the macrocyclic GBCA gadobutrol (0.1 mmol/kg of body weight) were retrospectively included in

45 with a mean blood glucose difference of 0.1 mmol/L (95% CI -0.6 to 0.7).

46 .2 mmol/L and 143.3 +/- 0.4 vs 138.8 +/- 0.1 mmol/L, respectively; p < 0.001 for both), but similar c

47 imum equilibrium CO2 capture capacity of 1.1 mmol g(-1) was achieved at 273 K.

48 .6) in the comparator period (difference 1.1 mmol/L, 95% CI 0.7-1.6; p<0.0001), and the mean time wit

49 ients when compared to controls (3.2 +/- 1.1 mmol/l, p < 0.001).

50 n the CGM plus CSII group and 0.1% (0.4; 1.1 mmol/mol [4.4]) in the CGM plus MDI group (p=0.32).

51 nonfasting plasma glucose >/=200 mg/dl (11.1 mmol/l), glycated hemoglobin A1c (HbA1c) >6.5%, self-rep

52 oncentrations (ie, higher or lower than 11.1 mmol/L).

53 od glucose level of 55 mg per deciliter (3.1 mmol per liter) or below was significantly lower in the

54 CI, -0.57% to -0.29%] or -4.7 [-6.3 to -3.1 mmol/mol]; P < .001).

55 those of gadopentetate dimeglumine (r1 = 4.1 mmol(-1) .

56 lipoprotein cholesterol >4.9 mmol/L or >4.1 mmol/L in combination with other risk factors received r

57 L-C significantly predicted death (HR:0.44/1 mmol/l, 95%CI:0.26-0.74, p = 0.002) after a median follo

58 (109 mg per deciliter [IQR, 102 to 118]; 6.1 mmol per liter [IQR, 5.7 to 6.6]) than in the higher-tar

59 trol: 80 to 110 mg per deciliter (4.4 to 6.1 mmol per liter; lower-target group) or 150 to 180 mg per

60 nitrite levels, e.g., [NO3(-)] approaching 1 mmol L(-1) (corresponding to approximately 60 mg L(-1)).

61 Decreases in serum total cholesterol >1 mmol/L >/=1 year prior to cancer diagnosis were associat

62 ; non-inferiority was deemed a difference <1 mmol/L).

63 ongevity (OR: 0.61; 95% CI: 0.35, 1.07 per 1 mmol/L increase in triglycerides).

64 1147, rs2479409, and rs11206510) scaled to 1 mmol/L lower LDL cholesterol showed associations with in

65 index (beta = 0.46; 95% CI: 0.14, 0.78 per 1-mmol/L increase) and risk of macrosomia (birth weight >4

66 4000 g) (RR = 1.21; 95% CI: 1.07, 1.38 per 1-mmol/L increase).

67 ndard care: 9.3 [1.8] vs liberal: 10.3 [2.1] mmol/L; p = 0.02) and nadir blood glucose (4.4 [1.5] vs

68 , 0.07 mmol/L), and 0.04 mmol/L (-0.02, 0.10 mmol/L); -0.08 mm Hg (-0.26, 0.11 mm Hg); and -1.0 mm Hg

69 d at-goal (all measurements >/=3.9 and </=10 mmol/L [>/=70 and </=180 mg/dL] during the pre-vGMS, tra

70 d running electrolyte (BGE) consisting of 10 mmol L(-1) N-cyclohexyl-2-aminoethanesulfonic acid (CHES

71 itive ionization mode, the application of 10 mmol/L ammonium formate led to the best findings, while

72 A reaction on 10 mmol scale further highlighted the practical utility of

73 in mean serum chloride concentration (per 10 mmol/L; odds ratio, 7.39; 95% CI, 3.44-18.23), but not s

74 sample and water or NH4OH solutions (10-100 mmol L(-1)) were investigated for analytes absorption.

75 The lowest chloride tertile (</=100 mmol/L) was associated with increased mortality rates in

76 o use diluted absorbing solutions (up to 100 mmol L(-1) NH4OH) for halogens retention, providing limi

77 ealthy controls and patients with AMN (0.102 mmol trolox equivalent; P < .01), as well as healthy con

78 oprotein (4 studies; mean differences, -0.11 mmol/L; 95% CI, -0.17 to -0.04), and blood glucose (2 st

79 mmol/L, 8 mmol/L, 9 mmol/L, 10 mmo/L, and 11 mmol/L respectively according to the guideline of WHO.

80 of moderate hyperchloremia (chloride >/= 115 mmol/L) on clinical outcomes in intracerebral hemorrhage

81 erol was higher by 43 mg per deciliter (1.12 mmol per liter) in the anacetrapib group than in the pla

82 at doses of gadodiamide (cumulative dose, 12 mmol per kilogram of body weight) by using inductively c

83 rates in the context of lower sodium (</=138 mmol/L; adjusted hazard ratio [95% confidence interval]

84 calcium was 0.35 +/- 0.17 and 0.38 +/- 0.14 mmol/L at 1 and 3 hours, respectively, within the extrac

85 lightly lowered fasting blood glucose (-0.14 mmol/L; 95% CI: -0.24, -0.036 mmol/L), HbA1c [-10 g/L (9

86 reduction of CO2 into CO ( approximately 14 mmol g(-1) h(-1) ) and high selectivity over CH4 (>96.4%

87 in the context of higher sodium levels (>141 mmol/L), the association with mortality was lost.

88 ed each of 3 sodium levels (50, 100, and 150 mmol/day at 2,100 kcal) in random order over 4 weeks sep

89 capacity is obtained in SIFSIX-2-Cu-i (4.16 mmol g(-1) SO2 at 0.01 bar and 2.31 mmol g(-1) at 0.002

90 L) (normal range, 13.5-18.0 g/dL [8.38-11.17 mmol/L]) and a bilirubin level of 62 micromol/L (normal

91 % CI: 1.2-, 2.9-kg) lower weight, and a 0.17-mmol/L (95% CI: 0.11-, 0.23-mmol/L) lower LDL cholestero

92 xcretion, ranging from 3.8 to 3.9 g (165-170 mmol), was equal among all methods (P=0.88).

93 glucose (2 studies; mean differences, -0.18 mmol/L; 95% CI, -0.29 to -0.07).

94 removal of trace C2 H2 from C2 H4 with 1.18 mmol g(-1) C2 H2 uptake capacity from a 1/99 C2 H2 /C2 H

95 equivalent) and heterozygote carriers (0.181 mmol trolox equivalent), and significant reductions were

96 erol (MD: -0.32 mmol/L; 95% CI: -0.46, -0.19 mmol/L).

97 eir ICU stay (113.4 +/- 0.6 vs 107.1 +/- 0.2 mmol/L and 143.3 +/- 0.4 vs 138.8 +/- 0.1 mmol/L, respec

98 oncentrations were 1 +/- 0.1 and 3.1 +/- 0.2 mmol/L, respectively.

99 -cholesterol concentrations of less than 0.2 mmol/L.

100 -cholesterol concentrations of less than 0.2 mmol/L; p=0.0012 for the primary endpoint, p=0.0001 for

101 Materials and Methods A total dose of 13.2 mmol per kilogram of body weight of each GBCA was admini

102 glucose level below 40 mg per deciliter (2.2 mmol per liter) (18 patients [5.2%] vs. 7 [2.0%], P=0.03

103 T at room temperature) of Fe-tCDTA (r1 = 2.2 mmol(-1) . sec(-1)) were approximately twofold and fivef

104 Forty severe hypoglycemic events (<2.2 mmol/L [<40 mg/dL]) occurred during the pre-vGMS period

105 patients with initial normal lactate (< 2.2 mmol/L), elevated lactate (>/= 2.2 to < 4 mmol/L), or se

106 ndom blood glucose concentration of 7.8-22.2 mmol/L who were being treated with diet or oral antidiab

107 (7.1 cf 8.6 mmol L), SD glucose (1.7 cf 3.2 mmol/L), and CONGA4 (1.6 cf 3.0).

108 was first demonstrated between 75 mg/dL (4.2 mmol/L) and 60 mg/dL (3.3 mmol/L) with increases in both

109 ge in CMRglc (P = 1.0) between 75 mg/dL (4.2 mmol/L) and 60 mg/dL (3.3 mmol/L), whereas CMRglc signif

110 tial-exponential phase then increased to 4.2 mmol/mol-C at death phase.

111 ith Septic Shock 3.0 definition (lactate > 2 mmol/L) differ from vasopressin versus norepinephrine an

112 I], 1.15-2.45; P = .007), serum lactate >/=2 mmol/L (HR, 2.13; 95% CI, 1.39-3.25; P < .001), and unkn

113 endent of portal ammonia concentrations </=2 mmol/L.

114 ith septic shock with lactate greater than 2 mmol/L or less than or equal to 2 mmol/L, randomized to

115 ess than or equal to 2 versus greater than 2 mmol/L.

116 sors, and exhibited a lactate greater than 2 mmol/L.

117 ess than or equal to 2 versus greater than 2 mmol/L.

118 n treatment groups in lactate greater than 2 mmol/L.

119 inephrine in lactate less than or equal to 2 mmol/L but no difference between treatment groups in lac

120 reater than 2 versus less than or equal to 2 mmol/L, a brisker cytokine response to infection.

121 ter than 2 mmol/L or less than or equal to 2 mmol/L, randomized to vasopressin or norepinephrine.

122 reater than 2 versus less than or equal to 2 mmol/L.

123 hrine if lactate was less than or equal to 2 mmol/L.

124 obtained when the sample was diluted with 2 mmol L(-1) HNO3 and then electro-oxidized by applying a

125 .13micromolg(-1)DM) and the concentration (2-mmol sodium selenate) above which the content of phenoli

126 nsive GLP-1 secretion in the ileum at >/=200 mmol/L glucose.

127 tional days, during which SCFA mixtures (200 mmol/L) high in either acetate (HA), propionate (HP), bu

128 In vivo, 200 mmol/L NaHCO3 added to the drinking water of 4-week-old

129 as shown between the healthy controls (0.225 mmol trolox equivalent) and heterozygote carriers (0.181

130 ight, and a 0.17-mmol/L (95% CI: 0.11-, 0.23-mmol/L) lower LDL cholesterol.

131 rger scale reactions (>/= approximately 0.25 mmol) were generally facile from CH2Cl2.

132 erol (MD: -0.35 mmol/L; 95% CI: -0.46, -0.25 mmol/L) and non-HDL cholesterol (MD: -0.32 mmol/L; 95% C

133 and a difference in fasting glycemia of 0.25 mmol/L.

134 our OGTT glucose concentrations (beta = 0.25 mmol/L; P = 0.02).

135 ucolipotoxicity (0.5 mmol/L palmitate and 25 mmol/L glucose) increases LC3 II, a marker of autophagy.

136 of 0.77 mmol-Na(+) per gram of cathode (2.29 mmol-Na(+) g-MnO2(-1)), and peak charge efficiency of 0.

137 ion regimes at lower concentrations (c = 0.3 mmol L(-1)), 315 nm irradiation leads to the highest con

138 0 hour, 10.5 +/- 0.8 vs 7 hours, 1.4 +/- 0.3 mmol/L, P < 0.001).

139 esterol level below 50 mg per deciliter (1.3 mmol per liter) at day 180.

140 concentrations between 0.5 and less than 1.3 mmol/L, 3444 (13%) patients achieved concentrations betw

141 by its ultrahigh water vapor uptake of 14.3 mmol g(-1) at low relative pressure of P/P0 = 0.4 and ul

142 with CGM glucose concentration less than 3.3 mmol/L was 0.6% (0.6) in the bionic pancreas period vers

143 y decreased (P = 0.02) between 60 mg/dL (3.3 mmol/L) and 45 mg/dL (2.5 mmol/L).

144 ween 75 mg/dL (4.2 mmol/L) and 60 mg/dL (3.3 mmol/L) with increases in both plasma epinephrine (P = 0

145 ween 75 mg/dL (4.2 mmol/L) and 60 mg/dL (3.3 mmol/L), whereas CMRglc significantly decreased (P = 0.0

146 ng (CGM) glucose concentration less than 3.3 mmol/L, analysed over days 2-11 in participants who comp

147 [<3.9 mmol/L], p=0.0002 for <60 mg/dL [<3.3 mmol/L], p=0.0009 for <50 mg/dL [<2.8 mmol/L], p=0.0002

148 m baseline to 28 weeks was 0.3% (SD 0.9; 3.3 mmol/mol [SD 9.8]) in the CGM plus CSII group and 0.1% (

149 HbA1c was 8.53% (70 mmol/mol; SD 0.67% [7.3 mmol/mol]).

150 e duodenum and ileum, but not the colon, 300 mmol/L glucose potently stimulated GLP-1 release.

151 levels in the comparison group (beta = 0.301 mmol/L per allele, p < 0.001), with an F statistic of 95

152 -i (4.16 mmol g(-1) SO2 at 0.01 bar and 2.31 mmol g(-1) at 0.002 bar).

153 5 mmol/L) and non-HDL cholesterol (MD: -0.32 mmol/L; 95% CI: -0.46, -0.19 mmol/L).

154 diabetes, as it can detect as small as 1.33 mmol/l (0.025 wt%) glucose concentrations in the control

155 ement, 50% of the subjects had a >0.8-g (>34-mmol) difference in sodium intake with long-term estimat

156 ificantly lowered LDL cholesterol (MD: -0.35 mmol/L; 95% CI: -0.46, -0.25 mmol/L) and non-HDL cholest

157 and HDL cholesterol concentrations were 2.35 mmol/L (91 mg/dL) and 1.0 mmol/L (39.5 mg/dL), respectiv

158 olesterol level of 92 mg per deciliter (2.38 mmol per liter), and a mean HDL cholesterol level of 40

159 rom receiver operating characteristics (2.39 mmol/L) showed strong negative prediction (99.28%), but

160 n baseline value of 92 mg per deciliter (2.4 mmol per liter) to 30 mg per deciliter (0.78 mmol per li

161 lycated hemoglobin decreased from 6.1 to 5.4 mmol/mol and 41.8% to 37.7%, respectively.

162 nferior to that in the basal-bolus group 9.4 mmol/L [2.7]) with a mean blood glucose difference of 0.

163 4 mmol/L), or severe hyperlactatemia (>/= 4 mmol/L), the frequency of citrate accumulation was 0.77%

164 s with initial severe hyperlactatemia (>/= 4 mmol/L), the median calculated lactate clearance at 6, 1

165 .2 mmol/L), elevated lactate (>/= 2.2 to < 4 mmol/L), or severe hyperlactatemia (>/= 4 mmol/L), the f

166 below the typical human glucose levels of 4 mmol/l.

167 ane oxygenation blood lactate greater than 4 mmol/L (2.6 [1.03-6.4]) as independent predictors of 1-y

168 a difference of 15.3 mg per deciliter (0.40 mmol per liter) (P=1.0x10(-16)), and a lower risk of cor

169 , enabling a high CO2 working capacity (2.42 mmol/g, 9.1 wt %) with a modest 60 degrees C temperature

170 terol was lower by 17 mg per deciliter (0.44 mmol per liter), a relative difference of -18%.

171 her in the metformin group (0.46 versus 0.44 mmol/L; P=2.4x10(-4)).

172 uction increased from approximately 3 to >45 mmol Fe(II) kg(-1) d(-1) over the experiment with a conc

173 mg/dL), a total serum calcium level of 2.46 mmol/L (reference range, 2.14-2.53 mmol/L), and a carcin

174 /L), HbA1c (ADA HbA1c cutoff 5.7-6.4% [39-46 mmol/mol] and International Expert Committee [IEC] HbA1c

175 ents with prediabetes (HbA1c 5.7-6.4% [39-46 mmol/mol] or FPG 5.6-6.9 mmol/L) at baseline.

176 Committee [IEC] HbA1c cutoff 6.0-6.4% [42-46 mmol/mol]), and 2 h glucose concentration (ADA and WHO 2

177 mm +/- 12; range, 6-35 mm), with a TSC of 47 mmol/kg +/- 8 (P = .002).

178 dical records, or baseline HbA1c of 6.5% (48 mmol/mol) or greater or fasting plasma glucose (FPG) of

179 d haemoglobin (HbA1c) of less than 6.5% (<48 mmol/mol) after at least 2 months off all antidiabetic m

180 a mean (SD) HbA1c level of 6.66 (0.73)% [49 mmol/mol].

181 Intravenous Pi loading (0.5 mmol) caused a transient rise in plasma Pi levels and cr

182 d primary islets with glucolipotoxicity (0.5 mmol/L palmitate and 25 mmol/L glucose) increases LC3 II

183 Treatment of myotubes with 0.5 mmol/L palmitate for 4 h, but not with oleate, promoted

184 -cholesterol concentrations of less than 0.5 mmol/L, 8003 (31%) patients achieved concentrations betw

185 tion (NEP) following grazing (24.7 vs. 119.5 mmol C m(-2) d(-1)) in a Caribbean Thalassia testudinum

186 tients with 2 or more glucose values of 12.5 mmol/L or greater (>/=225 mg/dL) (hyperglycemic) and/or

187 ts received 20 intravenous injections of 2.5 mmol gadolinium per kilogram (gadolinium-exposed group)

188 euglycemia (6.0 mmol/L) or hypoglycemia (2.5 mmol/L) for 1 h.

189 75, 60, and 45 mg/dL (5.0, 4.2, 3.3, and 2.5 mmol/L) in 18 healthy young adults.

190 ween 60 mg/dL (3.3 mmol/L) and 45 mg/dL (2.5 mmol/L).

191 of time with glucose concentration below 3.5 mmol/L was reduced by 65% (53-74, p<0.0001) and below 2.

192 erol 3.4-5.7 mmol/L and triglycerides </=4.5 mmol/L) from 45 sites in the USA and Puerto Rico.

193 reached 0.40-83.7, 0.03-6.24, and 0.24-45.5 mmol m(-2) d(-1) for nitrate, phosphate, and silicate, r

194 lf-measured plasma glucose target of 4.0-5.5 mmol/L [72-99 mg/dL]) for 30 weeks.

195 ns are kept within a narrow range of 3.5-5.5 mmol/L.

196 ting total cholesterol concentrations of 6.5 mmol/L or lower, and who were not taking a statin or fib

197 ntration in the sitagliptin-basal group (9.5 mmol/L [SD 2.7]) was not inferior to that in the basal-b

198 exyl-2-aminoethanesulfonic acid (CHES) and 5 mmol L(-1) sodium hydroxide (NaOH).

199 , and arterial blood lactate at admission >5 mmol/l.

200 onsistent with myrosinase activity below 3.5-mmol sodium selenate.

201 other patients (2.4[2.2-2.7] vs 2.3[2.1-2.5]mmol/l, p = 0.51).

202 20.6% (SD 24.4; mean absolute decrease 1.50 mmol/L [SD 1.92]); these reductions were maintained at w

203 Cells were incubated with EtOH (50 mmol/L), CSE (20-40 mug/mL), or both (CSE+EtOH), and ana

204 uced using calcium concentrations of 100-500 mmol/L and injection volumes 20%-80% of tumor volume.

205 s were a hemoglobin level of 10.5 g/dL (6.52 mmol/L) (normal range, 13.5-18.0 g/dL [8.38-11.17 mmol/L

206 l of 2.46 mmol/L (reference range, 2.14-2.53 mmol/L), and a carcinoembryonic antigen value of 2.69 mu

207 olesterol level of 61 mg per deciliter (1.58 mmol per liter), a mean non-HDL cholesterol level of 92

208 hemoglobin A1c (HbA1c) of at least 7.5% (58 mmol/mol) treated with multiple daily insulin injections

209 lycaemia in adults with HbA1c below 7.5% (58 mmol/mol).

210 MCL [+2.4 +/- 0.4 compared with +2.0 +/- 0.6 mmol . d(-1); time x condition (mixed-model analysis): P

211 rs, prior stroke, glucose at admission >10.6 mmol/l (191 mg/dl), creatinine at admission >132.6 mumol

212 [>13.9 mmol/L], p=0.04 for >300 mg/dL [>16.6 mmol/L], and p=0.02 for the area under the curve for 180

213 sterol level of >/=100 mg per deciliter [2.6 mmol per liter] and the median follow-up was 12 months),

214 17%) patients achieved concentrations of 2.6 mmol/L or higher.

215 derwent a hyperinsulinemic-hypoglycemic (2.6 mmol/L) clamp, either after a HIIT session or after seat

216 ic-euglycemic (5.0 mmol/L)-hypoglycemic (2.6 mmol/L) clamps in 11 healthy participants, 10 patients w

217 s with target LDL-c levels </=100 mg/dL (2.6 mmol/L) or LDL-c reductions of at least 30% were extract

218 concentrations between 1.8 to less than 2.6 mmol/L, and 4395 (17%) patients achieved concentrations

219 shed estimates of seagrass NEP (median: 20.6 mmol C m(-2) d(-1)), NEP in grazed Caribbean T. testudin

220 Total cholesterol level was 3.6 mmol/L (normal, <5.0 mmol/L).

221 were categorized as normoglycemic (FPG <5.6 mmol/L), prediabetic (FPG 5.6-6.9 mmol/L), or diabetic (

222 on by center (n = 8) and hyperglycemia (>5.6 mmol/L).

223 Oscore (0 cf 1085), mean glucose (7.1 cf 8.6 mmol L), SD glucose (1.7 cf 3.2 mmol/L), and CONGA4 (1.6

224 After 6 mmol of KNO3, systolic blood pressure was reduced by a m

225 At 6 mmol/L glucose, ANP readily elicited Ca(2+) influx in co

226 mol twice daily during week 1, followed by 6 mmol thrice daily during week 2.

227 at the threshold glucose concentration of 6 mmol/L and decreased KATP single-channel activity in bet

228 Subjects received 6 mmol twice daily during week 1, followed by 6 mmol thric

229 nadir blood glucose (4.4 [1.5] vs 5.5 [1.6] mmol/L; p < 0.01) were increased during the liberal peri

230 r day in the combined RS groups and 108+/-61 mmol Na(+) per day in the LS groups (P<0.001).

231 Mean HbA1c was 7.92% (63 mmol/mol) during continuous glucose monitoring use and 8

232 s reflected by urinary excretion of 174+/-64 mmol Na(+) per day in the combined RS groups and 108+/-6

233 tinuous glucose monitoring use and 8.35% (68 mmol/mol) during conventional treatment (mean difference

234 antly reduced fasting plasma glucose by 0.69 mmol/L [1.32; 0.07], glycosylated hemoglobin A1C by 0.37

235 31 mm +/- 24; range, 6-92 mm), the TSC of 69 mmol/kg +/- 10 was, on average, 49% higher than that in

236 (2.6 +/- 0.8 mmol/l) and CTEPH (2.7 +/- 0.7 mmol/l) patients when compared to controls (3.2 +/- 1.1

237 ither 90 to 150 mg per deciliter [1.0 to 1.7 mmol per liter] or >150 mg per deciliter, depending on t

238 g exposure to elevated extracellular Ca (2.7 mmol/L) and isoproterenol (0.25 mumol/L) to induce diast

239 s and dyslipidaemia (LDL cholesterol 3.4-5.7 mmol/L and triglycerides </=4.5 mmol/L) from 45 sites in

240 together with olefin capacities exceeding 7 mmol/g.

241 hina, and an upper threshold mu was set to 7 mmol/L, 8 mmol/L, 9 mmol/L, 10 mmo/L, and 11 mmol/L resp

242 Mean baseline HbA1c was 8.53% (70 mmol/mol; SD 0.67% [7.3 mmol/mol]).

243 5.3% were women, and mean HbA1c was 8.6% (70 mmol/mol).

244 diabetes who had HbA1c lower than 8.8% (<73 mmol/mol).

245 on and a remarkable H2 -evolution rate of 73 mmol gCdSe-1 h-1 (10x higher than bare CdSe NCs).

246 mass deposition, reaching a maximum of 0.77 mmol-Na(+) per gram of cathode (2.29 mmol-Na(+) g-MnO2(-

247 f 8.3% (SD 13.0; mean absolute decrease 0.77 mmol/L [SD 1.38]; p=0.0001).

248 mmol per liter) to 30 mg per deciliter (0.78 mmol per liter) (P<0.001).

249 els to a median of 30 mg per deciliter (0.78 mmol per liter) and reduced the risk of cardiovascular e

250 LDL-C was lower in both PAH (2.6 +/- 0.8 mmol/l) and CTEPH (2.7 +/- 0.7 mmol/l) patients when com

251 te excretion >20% with plasma phosphate <0.8 mmol/L) in 596 HIV-infected and 544 HIV-uninfected AGEhI

252 olesterol levels of 70 mg per deciliter (1.8 mmol per liter) or higher who were receiving statin ther

253 esterol level of >/=70 mg per deciliter [1.8 mmol per liter] and the median follow-up was 7 months),

254 concentrations between 1.3 and less than 1.8 mmol/L, 7471 (29%) patients achieved concentrations betw

255 duced by 65% (53-74, p<0.0001) and below 2.8 mmol/L by 76% (59-86, p<0.0001).

256 l participants underwent a hypoglycemic (2.8 mmol/L) clamp after performing a bout of HIIT on a cycle

257 [<3.3 mmol/L], p=0.0009 for <50 mg/dL [<2.8 mmol/L], p=0.0002 for the area over the curve for 70 mg/

258 res mean difference versus placebo was -20.8 mmol/L (95% CI -23.4 to -18.2, average absolute change a

259 eline were observed in sweat chloride (-24.8 mmol/L; 95% CI, -29.1 to -20.5; P < 0.0001), body mass i

260 (123 mg per deciliter [IQR, 108 to 142]; 6.8 mmol per liter [IQR, 6.0 to 7.9]; P<0.001).

261 The mean CGM glucose concentration was 7.8 mmol/L (SD 0.6) in the bionic pancreas period versus 9.0

262 7.0 mmol/L for fasting glucose and/or >/=7.8 mmol/L for 2-h post-glucose.

263 ncentrations of o-methylbenzaldehydes (c = 8 mmol L(-1)), photoligations with N-ethylmaleimide (possi

264 an upper threshold mu was set to 7 mmol/L, 8 mmol/L, 9 mmol/L, 10 mmo/L, and 11 mmol/L respectively a

265 diabetes who had HbA1c lower than 9.7% (<83 mmol/mol) or in women with type 1 diabetes who had HbA1c

266 e ratio of Zn(2+) to ligand from 0.5 to 0.85 mmol.

267 , with a baseline HbA1c of 7.0%-10.0% (53-86 mmol/mol).

268 n (+10.9 +/- 0.9 compared with +12.3 +/- 1.9 mmol . d(-1); time x condition: P = 0.45) repletion.

269 rol levels (median, 74 mg per deciliter [1.9 mmol per liter]).

270 [>10.0 mmol/L], p=0.02 for >250 mg/dL [>13.9 mmol/L], p=0.04 for >300 mg/dL [>16.6 mmol/L], and p=0.0

271 ycemic) and/or a glucose level less than 3.9 mmol/L (<70 mg/dL) (hypoglycemic) in the previous 24 hou

272 or the area over the curve for 70 mg/dL [3.9 mmol/L]).

273 hypoglycaemia (p=0.0001 for <70 mg/dL [<3.9 mmol/L], p=0.0002 for <60 mg/dL [<3.3 mmol/L], p=0.0009

274 and low-density lipoprotein cholesterol >4.9 mmol/L or >4.1 mmol/L in combination with other risk fac

275 fasting glucose concentration cutoff 5.6-6.9 mmol/L and WHO fasting glucose concentration cutoff 6.1-

276 A1c 5.7-6.4% [39-46 mmol/mol] or FPG 5.6-6.9 mmol/L) at baseline.

277 fasting glucose concentration cutoff 6.1-6.9 mmol/L), HbA1c (ADA HbA1c cutoff 5.7-6.4% [39-46 mmol/mo

278 (FPG <5.6 mmol/L), prediabetic (FPG 5.6-6.9 mmol/L), or diabetic (FPG >/=7.0 mmol/L).

279 hreshold mu was set to 7 mmol/L, 8 mmol/L, 9 mmol/L, 10 mmo/L, and 11 mmol/L respectively according t

280 increased (from 2.6[2.1-3.2] to 4.0[2.8-4.9]mmol/l, p = 0.01) in patients with PH reversal but remai

281 xhibit competitive CO2 capacities (0.67-0.91 mmol g(-1) at 25 degrees C and 0.15 bar), extraordinary

282 5% and of those with an LDL-C level of 4.92 mmol/L (190 mg/dL) or greater were estimated.

283 CI, 2.3% to 3.5%) had an LDL-C level of 4.92 mmol/L (190 mg/dL) or greater.

284 ipoprotein cholesterol (LDL-C) level of 4.92 mmol/L (190 mg/dL) or greater.

285 ol-binding protein/creatinine ratio >2.93mug/mmol and/or fractional phosphate excretion >20% with pla

286 fined to have a molecular weight (MW) of 1 g mmol-1.

287 lbuminuria (albumin/creatinine ratio >/=3 mg/mmol), and proximal renal tubular dysfunction (retinol-b

288 0.26/0.72 micromol/L and 3.39/4.30 micromol/mmol creatinine, respectively.

289 2.89/5.67 micromol/L and 39.7/33.9 micromol/mmol creatinine.

290 ction (median [interquartile range], 38.6 ng/mmol [19.7-72.5] vs 25.9 ng/mmol [16.1-45.8], P = 0.009)

291 range], 38.6 ng/mmol [19.7-72.5] vs 25.9 ng/mmol [16.1-45.8], P = 0.009).

292 l/mmol) versus 7.58 nmol/mmol (SD, 6.17 nmol/mmol), with a mean difference of 0.67 nmol/mmol (95% CI,

293 f 0.67 nmol/mmol (95% CI, -1.13 to 2.48 nmol/mmol; P = .46).

294 l/mmol (SD, 4.67 nmol/mmol) versus 7.58 nmol/mmol (SD, 6.17 nmol/mmol), with a mean difference of 0.6

295 l/mmol), with a mean difference of 0.67 nmol/mmol (95% CI, -1.13 to 2.48 nmol/mmol; P = .46).

296 UFC excretion: 6.91 nmol/mmol (SD, 4.67 nmol/mmol) versus 7.58 nmol/mmol (SD, 6.17 nmol/mmol), with a

297 fference in 24-hour UFC excretion: 6.91 nmol/mmol (SD, 4.67 nmol/mmol) versus 7.58 nmol/mmol (SD, 6.1

298 ased risk of colorectal cancer (OR, 0.89 per mmol/L increase; 95% CI, 0.87-0.91); the association was

299 holesterol (OR, 0.83; 95% CI, 0.74-0.92, per mmol/l increase) were associated with lower odds of any

300 holesterol (OR, 0.87; 95% CI, 0.80-0.95, per mmol/l increase), and low-density lipoprotein (LDL) chol