ライフサイエンスコーパス: min

1 onger for FUSE (15.8 min) than for FVC (12.0 min) (P = .03).

2 clotting time of human blood (115.0 +/- 16.1 min, p < 0.001) compared to WT PAEC (34.0 +/- 8.2 min).

3 imes were similar (21.2 min for FUSE vs 19.1 min for FVC; P = .32), but withdrawal time was significa

4 However, photoactivation approximately 1 min after the induction did not affect them, suggesting

5 moderate initial brain uptake (SUV, 1.9 at 1 min after injection) with a rapid washout.

6 was etched and treated with 0.3 M EDC for 1 min and then bonded with the primer-bonding agent.

7 atio can be recorded on a tissue sample in 1 min or less, which is in sharp contrast to the 20 min or

8 t affect them, suggesting that the initial 1 min of CaMKII activation is sufficient for inducing LTP

9 enerated micromolar level H2O2 during just 1 min of direct CAP treatment on these cells.

10 c below a few seconds and fluid after just 1 min) and displays decreasing stiffness and increasing fl

11 sin for which the search process is long ( 1 min vs. 33 min).

12 01) and 16 weeks (30.5 min [-11 to 54] vs -1 min [-19 to 7]; p=0.025).

13 w and the optimized time for treatment was 1 min.

14 changes in protein-RNA interactions within 1 min following stress imposition.

15 vity and efficiency (kinact/KI > 10(5) M(-1) min(-1)).

16 mic 60-min (18)F-AV45 (291 +/- 67 MBq) and 1-min (15)O-H2O (370 MBq) scans were obtained in 35 age-ma

17 (0-2 min) mediated by VAMP2 and second (2-10 min) and third phases (10-30 min) mediated by VAMP8.

18 r with radial compared to femoral access: 10 min versus 9 min (p < 0.0001) and 65 Gy.cm(2) versus 59

19 ate remained significantly impaired after 10 min of reperfusion after global ischemia.

20 3D scanning was performed 0, 1, 3, 5, and 10 min after light curing.

21 only 35% of unchanged parent remaining at 10 min.

22 After blue light irradiation for 10 min at 470 nm, the sample was reimaged and analyzed.

23 aration after heating at 55 degrees C for 10 min owing to sedimentation of LCMs.

24 ther TSCR rise, compared with cooling for 10 min.

25 is paper, we present a short immunoassay (10 min) using a fiber-optic surface plasmon resonance (FO-S

26 ations of Fe(2+) (10 and 20 mM) rapidly (<10 min) transformed jarosite to a green rust intermediary,

27 (4 mg/kg padeliporfin intravenously over 10 min and optical fibres inserted into the prostate to cov

28 r optogenetic C1 neuron (C1) stimulation (10 min) protected mice from ischemia-reperfusion injury (IR

29 0 nm; frequency: 30 KHz) during and up to 10 min after light curing.

30 plasma OT concentrations increased within 10 min after oral delivery in postnatal day 1-7 mice.

31 These reactions proceed within 10 min at room temperature, which represents among the mild

32 unctionalities in >99 % conversion within 10 min to 1 h.

33 th a low nanomolar detection limit within 10 min.

34 A 10-min loading dose of intravenous ghrelin/placebo (3 mcg k

35 n for hROIs, 60-80 min for lROIs, and 80-100 min for lROIs and hROIs.

36 8 for a 540 min analysis and 4610 for a 1040 min analysis.

37 st peak at 1-6 min and a second peak at 7-12 min after stimulation with forskolin.

38 onance angiography at baseline and after 120 min.

39 measured at baseline, 15, 30, 60, 90 and 120 min after feeding.

40 ng uptake of (18)F-DCFPyL between 60 and 120 min after injection in 203 lesions characteristic for pr

41 F-DCFPyL (n = 62, 269.8 MBq, PET scan at 120 min after injection) or (68)Ga-PSMA-HBED-CC (n = 129, 15

42 ardium showed decreased contractility at 120 min- and 24 h-CMR accompanied by transient alterations i

43 underwent dynamic PET imaging for up to 120 min after bolus injection of (18)F-T807 with arterial bl

44 h the results of the full acquisition (0-140 min).

45 ference standards for all values was 120-140 min for hROIs, 60-80 min for lROIs, and 80-100 min for l

46 harge before [baseline (BL)], during, and 15 min after three 5 min hypoxic episodes (11% O2, H1-H3).

47 in LS174T tumors was observed as early as 15 min after injection (9.2 +/- 2.0 percentage injected dos

48 (25 mg/L) alone, and their combination at 15 min, 1 hr and 4 hr (n = 4).

49 mbrane-impermeable E2 (BSA-conjugated E2; 15 min).

50 ter group, connectivity remained elevated 15 min post-AIH (30%; p = 0.0002).

51 anodomains in PSDs, which were stable for 15 min or longer.

52 nts were prepared in batches of 49 in 1 h 15 min, which allowed for rapid prototyping and testing of

53 onor to acceptor solution was obtained in 15 min.

54 ll analyses can be completed in less than 15 min.

55 lyst loading and generally occurre within 15 min at room temperature for a range of activated alkenes

56 in stem cell mobilization peaking within 15 min that was equivalent in magnitude to a standard multi

57 d kinase (ERK), and Akt (occurring within 15 min).

58 Our results revealed that, within 15 min, NEM increased cell surface levels of KCC2 and modul

59 within 5 s and a stable Zre signal within 15 min.

60 In 65 unmedicated depressed patients 15-min resting-state EEGs were recorded off medication (bas

61 AP and LS values returned to baseline by 150 min.

62 ters were repeated every 30 min during a 150-min period.

63 At regular intervals over 180 min, appetite (visual analog scales), gastric emptying (

64 etion kinetics identified a first phase (0-2 min) mediated by VAMP2 and second (2-10 min) and third p

65 e total colonoscopy times were similar (21.2 min for FUSE vs 19.1 min for FVC; P = .32), but withdraw

66 p < 0.001) compared to WT PAEC (34.0 +/- 8.2 min).

67 yment in the system vibrated briefly every 2 min, while none of the congeners achieved more than 50%

68 ive measurements of primary metabolites in 2 min runs.

69 tracer, a head-to-thigh static scan with a 2-min acquisition per bed position was obtained.

70 Contractions peak after 15-20 min, but diminish by tenfold after 4 h.

71 4.2 percentage injected dose per gram by 20 min.

72 min of induced limb ischaemia and during 20 min of recovery after ischaemia.

73 Additional series of experiments (20 min in duration to ensure all animals survived) were stu

74 During the first 20 min of the FSIGT, plasma insulin was approximately twice

75 atalyst, aldehyde, and amine to react for 20 min before addition of the diazo compound.

76 m sample incubation to signal analysis of 20 min.

77 and 2, a lipid emulsion was given with or 20 min before the meal.

78 r less, which is in sharp contrast to the 20 min or more required by histopathological examination of

79 All participants underwent a 20-min PET acquisition 2 h after injection of 250 MBq of (1

80 pairment in mGlu3-LTD following a single, 20-min restraint stress exposure.

81 oducible when calculated from a truncated 20-min dataset.

82 The current density was maintained for >200 min at a constant potential while intermittently collect

83 e was quantified from a buffet meal (180-210 min; energy intake, appetite, and gastric emptying in th

84 53 nm with a fixed power of 150 mW/cm for 22 min 15 s) or active surveillance.

85 100% of 26 episodes with a median AFT of 22 min.

86 enyl ether at ca. 150-250 degrees C for 5-25 min affords in most cases the 1,3-diaryl-1,4-dihydrobenz

87 zed filopodia dynamics in HeLa cells over 25 min at 0.5 s temporal resolution, and visualized dynamic

88 /km) in the morning peak and from 2.8 to 5.3 min/km in the evening peak.

89 leaves to be estimated, calculated to be 8.3 min (combined residence times of root and stem) and 1.9

90 MBF was measured using (82)Rb injected 3 min after the beginning of hypercapnia and a 1-tissue-co

91 ions (25 degrees C, air flow rate of 1 cm(3) min(-1)).

92 , cytosolic Zn(2+) rises persisted for 10-30 min after OGD, followed by recovery over approximately 4

93 nd second (2-10 min) and third phases (10-30 min) mediated by VAMP8.

94 During a 30 min treatment, the PFOA concentration in 1.4 L of aqueou

95 anol-induced NREM sleep when administered 30 min prior to (but not after) ethanol injection.

96 al magnetic stimulation for approximately 30 min over the hand representation of the motor cortex at

97 nd MA1 graphical methods became linear by 30 min, yielding regional estimates of VT in excellent agre

98 VRCs were assessed at rest, during 30 min of induced limb ischaemia and during 20 min of recov

99 eart rate variability were assessed every 30 min and corrected QT intervals and T-wave morphology eve

100 and plasma parameters were repeated every 30 min during a 150-min period.

101 ime moving: +44%) shortly after exposure (30 min), and impaired motor functions (falls: +83%; time to

102 into control (RAMT(-)) or RAMT(+) groups (30 min daily RAMT over the stroke-affected gastrocnemius) a

103 gradual decrease in H2O2 concentration (>30 min) to almost zero as lactate was produced, and a subse

104 as it requires high temporal resolution(<30 min) and high fidelity rainfall recordings.

105 and reproducible peptide recovery in only 30 min.

106 lphalan at 200 mg/m(2) intravenously over 30 min on 1 day, followed by ASCT (control group).

107 Study participants received 30 min of real or sham transcranial direct current stimulat

108 ample to diagnostic readout, is less than 30 min, which allows the development of a point-of-care tes

109 esults for some isolates after only 10 to 30 min incubation.

110 traveling wave moved up to 450 mum within 30 min, while the gradient length remained 20 mum over this

111 ch that the APC is fully inhibited within 30 min.

112 pants were randomly assigned to iCST (75, 30-min sessions) or treatment as usual (TAU) control over 2

113 ts received gemcitabine 1000 mg/m(2) as a 30-min intravenous infusion, weekly, for 7 weeks followed b

114 usion every 8 h) or 1000 mg meropenem (by 30-min intravenous infusion every 8 h) for 7-14 days; regim

115 h the search process is long ( 1 min vs. 33 min).

116 .46 min vs 1.33 +/- 0.52 h and 2.04 +/- 0.36 min).

117 adjusted pH of 5.4 and a flow rate of 0.36mL/min.

118 er image can be processed in approximately 4 min.

119 tic stress relaxation has a lower bound of 4 min, which is comparable to the time required for intern

120 rine enantiomer as target compound in only 4 min.

121 5 weeks (median 70 min [IQR 32 to 151] vs 4 min [-21 to 18]; p<0.0001) and 16 weeks (30.5 min [-11 t

122 -heterocycles within short time spans (20-40 min).

123 required a single experiment of about 20-40 min.

124 ween intravenous ketamine (0.5 mg/kg over 40 min) and placebo (normal saline) on social phobia sympto

125 changes were evaluated after 8 sessions (40 min per session) of dichoptic training with the computer

126 uided detailed descriptions lasting up to 40 min.

127 m diluted blood serum was achieved within 40 min.

128 The process proceeds quickly (30-45 min) via in situ formation and intramolecular cyclizatio

129 ure implicated in extinction, before four 45-min or immediately after four 30min extinction sessions,

130 i DSM1103 (6.64 +/- 0.63 h and 2.85 +/- 0.46 min vs 1.33 +/- 0.52 h and 2.04 +/- 0.36 min).

131 lation, but the short-lived (51)Mn (t1/2: 46 min, beta(+): 97%) represents a viable alternative.

132 that fluctuate rapidly on timescales of <1.5 min.

133 he periphery after exposure to CSF-1 for 2.5 min was shown by immunofluorescence microscopy.

134 The reduction in hands on time was 25.5 min per culture.

135 in [-21 to 18]; p<0.0001) and 16 weeks (30.5 min [-11 to 54] vs -1 min [-19 to 7]; p=0.025).

136 It was analyzed after 5 min by instant thin-layer chromatography and high-perfor

137 (infant and stillbirth), Apgar score <7 at 5 min, and admission to the neonatal unit.

138 The duration of a run averaged 5 min.

139 tin cytoskeleton remodels during the first 5 min of innate immune signaling in Arabidopsis (Arabidops

140 cid (100 mM, 1.0 wt%) at 120 degrees C for 5 min removed 85.7% of the xylan and 90.4% of the lignin l

141 evels of BPA (isotope-labeled BPA-d16) for 5 min, followed by hand-washing 2 h later.

142 line (BL)], during, and 15 min after three 5 min hypoxic episodes (11% O2, H1-H3).

143 icles, in the range of 200-500-fold within 5 min.

144 ation produces >50% compromised DNA within 5 min.

145 Participants viewed a 50-min movie, then verbally described the events during fun

146 Peak capacity was 4018 for a 540 min analysis and 4610 for a 1040 min analysis.

147 GLP-1 is biphasic, with a first peak at 1-6 min and a second peak at 7-12 min after stimulation with

148 vinyllysine (Ki = 470 +/- 30 muM; t1/2 = 3.6 min).

149 n compared to a standard immunoassay, in a 6 min protein-antibody reaction.

150 es at a time, takes place in approximately 6 min, with approximately 50% cell capture efficiency.

151 ulation reached 80% dissolved in less than 6 min whereas the equivalent marketed liquid filled nifedi

152 Imaging was performed at rest and during 6-min hypercapnic plateaus (baseline; PETco2 at 50, 55, an

153 r hospitalizations, and percent changes in 6-min walk distance) at 6 months.

154 a Living with Heart Failure Questionnaire, 6-min walk test, major adverse cardiac events, and immune

155 lycosomes, and can be visualized after 30-60 min.

156 injected dose per cubic centimeter at 40-60 min and rapid clearance from blood to kidney and bladder

157 ollowed by recovery over approximately 40-60 min.

158 Blood metabolite analysis 60 min after injection of the tracer showed a 2.5-fold incr

159 cortisol (change in baseline cortisol at 60 min of < 9 mug/dL) after cosyntropin (250 mug) administr

160 QT intervals and T-wave morphology every 60 min.

161 erelaxin intravenous (i.v.) infusion (for 60 min at 80 mug/kg/d and then 60 min at 30 mug/kg/d) or te

162 Prolonged cooling, for 60 min, was associated with a further TSCR rise, compared w

163 ntinuous or >/=3 h) versus short-term (</=60 min) infusion of antipseudomonal beta-lactams for the tr

164 (68)Ga-PSMA-HBED-CC (n = 129, 158.9 MBq, 60 min after injection).

165 y to ascend: +280%) over a longer period (60 min).

166 usion (for 60 min at 80 mug/kg/d and then 60 min at 30 mug/kg/d) or terlipressin (single 2-mg i.v. bo

167 s) and multiparous mice were subjected to 60 min of reversible middle cerebral artery occlusion and e

168 SUVmax analyses were based on uptake 60 min after tracer injection, and volumetric CT histogram

169 Dynamic 60-min (18)F-AV45 (291 +/- 67 MBq) and 1-min (15)O-H2O (370

170 fixed-ratio 20 schedule of reinforcement (60-min sessions once a day, 5 days per week).

171 From 360-600 min, the remaining dogs underwent a hyperinsulinemic (4x

172 r-to-brain ratios of (18)F-FET uptake (18-61 min after injection) were evaluated using a volume-of-in

173 time at the initial surgery (median 76 vs 66 min, P < 0.01), but a lower re-excision rate for positiv

174 Imaging started at 40-69 min (mean, 50.5 +/- 6.8 min) after injection of 133.2-15

175 armed saline (15 mL kg(-1) , approximately 7 min).

176 The assay was completed in <7 min.

177 ric emptying of solids at 5 weeks (median 70 min [IQR 32 to 151] vs 4 min [-21 to 18]; p<0.0001) and

178 time was significantly longer for FUSE (15.8 min) than for FVC (12.0 min) (P = .03).

179 vinyllysine (Ki = 630 +/- 20 muM; t1/2 = 2.8 min) and D-alpha-(1'-fluoro)vinyllysine (Ki = 470 +/- 30

180 ing started at 40-69 min (mean, 50.5 +/- 6.8 min) after injection of 133.2-151.7 MBq (mean, 140.6 +/-

181 ly following glucose withdrawal (0, 4, and 8 min).

182 d to tandem mass spectrometry in less than 8 min.

183 all values was 120-140 min for hROIs, 60-80 min for lROIs, and 80-100 min for lROIs and hROIs.

184 2 day introductory workshop and gave nine 80 min lessons during one school term.

185 ificity to the species level in less than 80 min with the limits of detection at 1 x 10(3) to 10 x 10

186 ed residence times of root and stem) and 1.9 min mm(-1) leaf, respectively.

187 Within a total residence time of 9 min, the sodium salt of ciprofloxacin was prepared from

188 in primary mouse hippocampal neurons over 9 min at 2 s temporal resolution.

189 compared to femoral access: 10 min versus 9 min (p < 0.0001) and 65 Gy.cm(2) versus 59 Gy.cm(2) (p =

190 educed that of alpha-lactalbumin (only at 90 min) (P < 0.05).

191 Using 90 min analyses we show that AI-ETD can identify 24,503 loc

192 tely determine drug susceptibility within 90 min.

193 with PD and 10 healthy subjects underwent 90-min dynamic PET.

194 rtile] time expending >/=3 METs, 46 [21, 92] min) were enrolled and assigned to the intervention (n =

195 he natural logarithmic pre-exponential ln (A/min(-1)) factors of ca. 19-35 and 28-41, in the same ord

196 = .80), maximum heart rate (174 vs 175 beats/min; P = .41), and heart rate at 2 minutes recovery (44

197 t rate at 2 minutes recovery (44 vs 43 beats/min; P = .28).

198 A heart rate <70 beats/min was also associated with a lower risk for the combin

199 ients with heart rate <70 versus >/=70 beats/min, balanced on 58 baseline characteristics.

200 ty scores for discharge heart rate <70 beats/min, estimated for each of the 6,286 patients, were used

201 discharge heart rate <70 versus >/=70 beats/min, respectively (hazard ratio [HR]: 0.86; 95% confiden

202 relative bradycardia (heart rate, < 80 beats/min) in septic shock are unknown.

203 he estimated RR and TV values were 0 breaths/min and less than 100 ml, respectively.

204 ion, attaining peak rates of 1.57 +/- 0.32 g min(-1) during 2 h of walking at approximately 80% VO2 p

205 eline oxygen delivery less than 4.5 mL/100 g/min.

206 consumption, 24+/-1.3 versus 31+/-1.3 mL/kg/min, P<0.001; increased VE/Vco2 slope, 31+/-1 versus 26+

207 tinuous ghrelin/placebo infusion (16.9 ng/kg/min) was administered.

208 rose from 2.1 to 3.1 minutes per kilometer (min/km) in the morning peak and from 2.8 to 5.3 min/km i

209 9 L/min at baseline compared to 6.5 +/-2.1 L/min at follow-up, P = 0.66.

210 oxygen saturation was 93% or less and at 2 L/min if oxygen saturation was greater than 93%.

211 - 1.7 L/min at baseline versus 6.9 +/- 2.3 L/min at follow-up, compared to placebo, mean 6.6 +/- 1.9

212 Oxygen was given via nasal tubes at 3 L/min if baseline oxygen saturation was 93% or less and at

213 found on cardiac output, mean 6.9 +/- 1.7 L/min at baseline versus 6.9 +/- 2.3 L/min at follow-up, c

214 -up, compared to placebo, mean 6.6 +/- 1.9 L/min at baseline compared to 6.5 +/-2.1 L/min at follow-u

215 eserved (cardiac index 2.8+/-0.6 [1.9-3.9] L/min per m(2)), and diastolic function mildly abnormal.

216 low and uniform-flow) and two realistic (max-min fairness and proportional fairness) congestion contr

217 Participants in the >2000 MET-min/wk group had a higher prevalence of CAC and atherosc

218 gorized as <1000, 1000 to 2000, or >2000 MET-min/wk.

219 .02 +/- 2.0 compared with -0.03 +/- 2.8 mg . min(-1), respectively; P = 0.9) or first-phase insulin s

220 g10 RT-qPCR reduction between 300 and 360 mg-min/L.

221 T values for both disinfectants up to 450 mg-min/L.

222 uptake from the CVVH circuit was 60 +/- 2 mg/min and provided 218 +/- 8 kcal/d.During CVVH there was

223 wide range of TRBF from 31.1 to 75.0 microL/min, with the distribution being highly skewed.

224 usion of 1-2 ml of fresh blood at 200 microl/min over cortical sulci caused clusters of spreading dep

225 F patients were 68+/-11 years and 78+/-14 mL min(-1) 1.73 m(-2) and in patients without HF were 59+/-

226 without HF were 59+/-14 years and 84+/-16 mL min(-1) 1.73 m(-2), respectively.

227 d glomerular filtration rate (eGFR) >/=60 mL min(-1) 1.73 m(-2) during October 1, 2004 to September 3

228 ; peak oxygen consumption: 66.8 +/- 1.3 mL . min(-1)) were studied twice.

229 perating characteristic curve (AUC, in g/mL. min) for (18)F-FTT was assessed in normal mouse organs b

230 estimated glomerular filtration rate <20 mL.min(-1).1.73 m(-2), or dialysis.

231 7.7+/-2.3 versus 10.0+/-3.4 and12.9+/-4.0 mL/min.kg; P<0.0001), higher biventricular filling pressure

232 .20) and an annual decrease in eGFR of >1 ml/min per 1.73 m(2) (odds ratio, 3.64; 95% confidence inte

233 dent eGFR <60 ml/min per 1.73 m(2) and >1 ml/min per year decline) were evaluated.

234 a continuous and ultrahigh-throughput (>1 mL/min) manner.

235 .9 mL/min/g and adenosine was 2.2 +/- 1.1 mL/min/g; these were significantly higher than at rest (0.9

236 ysis rates of 100K/s and flow rates of 10 mL/min, while maintaining optical performance comparable to

237 tal vein at three flow rates (60, 80, 100 mL/min per 100 g of liver) was used.

238 notic kidney RBF rose (202+/-29-262+/-115 mL/min; P=0.04) 3 months after PTRA in the elamipretide-tre

239 on was larger in hyperfiltering (GFR >120 mL/min) than nonhyperfiltering patients and was associated

240 te maximal hyperemia at a flow rate >/=15 mL/min.

241 ikely to cause clotting compared with 150 mL/min (hazards ratio, 1.00 [0.60-1.69]; p = 0.68).

242 = 47) using 462 circuits (245 run at 150 mL/min and 217 run at 250 mL/min).

243 domized with 96 completing the study (150 mL/min, n = 49; 250 mL/min, n = 47) using 462 circuits (245

244 ith greater eGFR decline (-1.12 and -0.18 ml/min per 1.73 m(2) per year, respectively; P=0.02 and P<0

245 m in the SRL/MMF group and 59.2 +/- 27.2 mL/min/1.73 m in the CNI/MMF group and was not statisticall

246 5 and 10 years; and 0.07 (-0.10 to +0.25) mL/min/1.73m((2)) /yr between 10 and 20 years for donors wi

247 therapy using blood flow rate set at 250 mL/min was not more likely to cause clotting compared with

248 (245 run at 150 mL/min and 217 run at 250 mL/min).

249 leting the study (150 mL/min, n = 49; 250 mL/min, n = 47) using 462 circuits (245 run at 150 mL/min a

250 >/=30%; absolute decline: eGFR decline >3 ml/min per year) and incident CKD (incident eGFR <60 ml/min

251 tive risks for 12-month eGFR less than 30 mL/min per 1.73 m were 1.9 (1.2-3.1) and 2.1 (1.1-3.7), wit

252 mong patients with preoperative eGFR>/=30 ml/min per 1.73 m(2), the incidence of CKD stage 4 or highe

253 estimated glomerular filtration rate <30 mL/min per 1.73m(2), or development of overt diabetic nephr

254 sustained reduction in eGFR less than 30 mL/min/1.73 m2 for at least 3 months during the year after

255 ate of change in eGFR (-0.47 versus -0.32 ml/min per 1.73 m(2) per year; P<0.03).

256 reached age 70: 1.12 (95% CI: 0.92-1.32) mL/min/1.73m((2)) /yr between 6 weeks and 5 years postdonat

257 tients with baseline eGFR greater than 40 mL/min/1.73 m2, higher log-transformed suPAR levels were as

258 nd 5 years postdonation; 0.24 (0.00-0.49) mL/min/1.73m((2)) /yr between 5 and 10 years; and 0.07 (-0.

259 = 34; CNI/MMF, n = 26) was 63.2 +/- 28.5 mL/min/1.73 m in the SRL/MMF group and 59.2 +/- 27.2 mL/min

260 ficantly higher than at rest (0.9 +/- 0.5 mL/min/g, P < 0.05) and were not different from each other

261 ograf using observed values (47.7 vs 38.6 mL/min per 1.73 m, P < 0.001) and was superior based on obs

262 independently associated with an eGFR<60 ml/min per 1.73 m(2) (odds ratio, 6.85; 95% confidence inte

263 We defined incident CKD as eGFR<60 ml/min per 1.73 m(2) and >/=30% eGFR decline at the third v

264 year) and incident CKD (incident eGFR <60 ml/min per 1.73 m(2) and >1 ml/min per year decline) were e

265 ose participants with baseline eGFR >/=60 ml/min per 1.73 m(2) At baseline, mean age was 55 years old

266 d 1.5-3.5 mg/dl for men (or eGFR of 20-60 ml/min per 1.73 m(2)), and a 24-hour urine protein-to-creat

267 duals with moderately reduced eGFR (30-60 ml/min per 1.73 m(2)).

268 68% of PEPT2*1*1 carriers had an eGFR<60 ml/min per 1.73 m(2), compared with 37% of PEPT2*1*2 carrie

269 d glomerular filtration rate less than 60 mL/min per 1.73 m.

270 lar filtration rate (eGFR) of at least 60 mL/min/1.73 m2.

271 ith CKD G3aA1 by eGFRcreat to eGFR >/= 60 ml/min/1.73 m2.

272 nd cyclosporine were 67.0, 68.7, and 42.7 mL/min per 1.73 m(2) , respectively (P<.001 for overall tre

273 filtration rate (eGFR) was 33.9 +/- 15.8 ml/min/1.73 m(2) and the median urinary protein-to-creatini

274 ximal hypercapnic stimulus (2.00 vs. 0.86 mL/min/g; P < 0.0001).

275 ean MBF under hypercapnia was 2.1 +/- 0.9 mL/min/g and adenosine was 2.2 +/- 1.1 mL/min/g; these were

276 rticipants were men, and mean eGFR was 94 ml/min per 1.73 m(2) Over a median follow-up of 8 years, 22

277 th estimated glomerular filtration rates (mL/min per 1.73 m) of 43 to 72 (median, 55).

278 tides tested at flow rates from 15 to 55 muL min(-1).

279 apid mixing (71% +/- 12% after 5 mm, 100 muL/min) was observed, indicating a strength in fabricating

280 les and at flow rates of 25, 50, and 100 muL/min.

281 the volumetric rate to approximately 250 muL/min.

282 w rates ( approximately 50 nL/min to 500 muL/min) to accommodate both low- and high-flow MS ionizatio

283 M value of 3 +/- 2 mM (Vmax, 900 +/- 300 muM/min) for 3'-sialyllactose.

284 a range of flow rates ( approximately 50 nL/min to 500 muL/min) to accommodate both low- and high-fl

285 tyl expressing GFP-AtCESA6 was 184 +/- 86 nm min(-1) (n = 2755).

286 tely 10(8) to approximately 10(11) particles min(-1), and the rates varied over the course of a print

287 eration basin and 79 PFU min(-1) and 0.3 PFU min(-1) for the sewer pipes.

288 emission rates of MS2 and Phi6 were 547 PFU min(-1) and 3.8 PFU min(-1), respectively, for the aerat

289 pectively, for the aeration basin and 79 PFU min(-1) and 0.3 PFU min(-1) for the sewer pipes.

290 S2 and Phi6 were 547 PFU min(-1) and 3.8 PFU min(-1), respectively, for the aeration basin and 79 PFU

291 melatonin synthesis were 500 muM and 12 pmol/min.mg protein, respectively.

292 Esophageal pressure-time product/min decreased from 165 (126-179) to 72 (54-137) cm H2O *

293 L h is only determined by L h2 when Q r < Q min < Q max (Case III).

294 it based on rated pump power (L h2 ); when Q min < Q max < Q r (Case II), L h is exclusively controll

295 Results show that when Q min </= Q r </= Q max (Case I), L h depends both on hori

296 from 165 (126-179) to 72 (54-137) cm H2O * s/min, respectively (p = 0.033).

297 Concealed vasopressin (0.03 U/min.) or norepinephrine infusions.

298 under the concentration-time curve 6 mg/mL x min; trastuzumab 8 mg/kg loading dose, 6 mg/kg maintenan

299 and high-dose subgroups (37.2 +/- 7.8 nmol x min(-1) x g(-1), P < 0.01 vs. controls, P < 0.05 vs. sta

300 alue in the standard-dose (27.9 +/- 9 nmol x min(-1) x g(-1), P < 0.05 vs. controls) and high-dose su