ライフサイエンスコーパス: potassium concentration

1 l membrane region over a wide range in serum potassium concentration.

2 lar Ca(2+) and depended on the extracellular potassium concentration.

3 space, and an increase in the extracellular potassium concentration.

4 therapy was independent of the initial serum potassium concentration.

5 iety of medications that can alter the serum potassium concentration.

6 ructural heart disease and an abnormal serum potassium concentration.

7 nscription induced by lowering extracellular potassium concentration.

8 ion for controlling blood pressure and serum potassium concentration.

9 ian manner with changes in the extracellular potassium concentration.

10 rnstian manner with changes in extracellular potassium concentration.

11 of membrane potential and the extracellular potassium concentration.

12 assium transport, and unresponsive to plasma potassium concentration.

13 ous infections leads to an increase in serum potassium concentration.

14 e cochlea, they promptly die due to the high potassium concentration.

15 anes, and (iii) a reduction in intracellular potassium concentration.

16 bsorbance and fluorescence) according to the potassium concentration.

17 C is mediated by secondary changes in plasma potassium concentration.

18 rough repetitive elevations of extracellular potassium concentration.

19 of binding was demonstrated with increasing potassium concentrations.

20 ertension are now known to have normal serum potassium concentrations.

21 l non-haemolysed blood samples showed normal potassium concentrations.

22 sium induced by CA, Ucn2 cotreatment reduced potassium concentrations.

23 e for doing so effectively across a range of potassium concentrations.

24 95% CI: -4.80, -1.09; P-trend: 0.01); higher potassium concentration (0.11 mEq/L; 95% CI: 0.03, 0.19;

25 The diarrheal fluid had a very high potassium concentration (130-170 mEq/L) and a very low s

26 atio (UACR) of >100-<=5000 mg/g, and a serum potassium concentration 3.5-5.0 mmol/L were randomly ass

27 Serum potassium concentration, 3-d food records, and 24-h urin

28 ed that in patients with hyperkalemia (serum potassium concentration 5.10-6.50 mmol/l [5.1-6.5 mEq/l]

29 nts with diabetes had a slightly higher peak potassium concentration (5.14 +/- 0.45 mmol/L [CI, 4.93

30 (1.2 mg/dL) or more developed a higher peak potassium concentration (5.37 +/- 0.59 mmol/L [CI, 5.15

31 Extracellular potassium concentration affects the membrane potential o

32 The elevated potassium concentration also depolarized the postsynapti

33 associated with an increase in extracellular potassium concentration and neuronal depolarization bloc

34 otassium buffering, increasing extracellular potassium concentration and overactivating the Na(+)-K(+

35 terized by a large increase of extracellular potassium concentration and prolonged subsequent electri

36 that KinC responds to lowered intracellular potassium concentration and that this is a quorum-sensin

37 (TBI) can be predicted by the extracellular potassium concentration and the change in energy homeost

38 o observed a significant correlation between potassium concentration and the weight of the mice.

39 Potassium concentration and transmembrane potential reco

40 e mechanisms by which DCT cells sense plasma potassium concentration and transmit the information to

41 reasing trends in total protein, albumin and potassium concentrations and an average increase of tota

42 atment and control groups had the same serum potassium concentrations and did not receive different a

43 iments performed under different calcium and potassium concentrations and in the presence of dextran

44 roximations, the transient solutions for the potassium concentrations and the corresponding membrane

45 which ictal activity was induced by elevated potassium concentrations and the fractional decrease in

46 population, there is no correlation between potassium concentrations and the occurrence of premature

47 hanism, inhibition was dependent on voltage, potassium concentration, and a histidine in the first P

48 duces no or only trivial reductions in serum potassium concentration, and because this therapy is unp

49 uch as mean predialysis serum phosphorus and potassium concentration, and behavioral compliance were

50 ll clinical scenario when choosing dialysate potassium concentrations, and an effective change in pra

51 changes in intracellular sodium or external potassium concentrations, and did not reflect a change i

52 imbalances, such as increased magnesium and potassium concentrations, and to cold shock, but increas

53 , which has highly dynamic tissue sodium and potassium concentrations, and we report 2 times relative

54 when extracellular sodium and intracellular potassium concentrations are within physiological ranges

55 lyte abnormalities, including abnormal serum potassium concentrations, are considered a correctable c

56 The increase in the extracellular potassium concentration associated with that wave leads

57 one, rats in the POL group had higher plasma potassium concentrations at 2 wk.

58 onse of the ECL intensity to the logarithmic potassium concentration between 10 mum and 10 mM was fou

59 l phosphorus concentration by 87.6% and soil potassium concentration by 38.0% compared to not using b

60 Insulin administration lowers plasma potassium concentration by augmenting intracellular upta

61 the liver, that buffer the changes in plasma potassium concentration by means of transcellular potass

62 es are thought to regulate the extracellular potassium concentration by mechanisms involving both vol

63 ontrast, treatment with an elevated external potassium concentration caused only a moderate increase

64 None of the regimens reduced serum potassium concentrations, compared with baseline levels.

65 Mean serum potassium concentrations decreased from 4.9 mmol/L to 4.

66 of renal potassium conservation when plasma potassium concentration decreases.

67 The range of potassium concentrations detected by an RNA G-quadruplex

68 sed potassium intake in the HKD group, serum potassium concentrations did not significantly increase

69 y, the effects of an increased extracellular potassium concentration diffusing in space-that support

70 Changes in the sample potassium concentration directly modulate the potential

71 ith a stimulus-induced rise in extracellular potassium concentration during stimulation.

72 e at rat carotid bodies superfused with high potassium concentrations, during normoxic hypercapnia, a

73 prophylaxis, supplementation only when serum potassium concentration fell below 3.6 mEq/L was noninfe

74 tassium control (only supplementing if serum potassium concentration fell below 4.5 mEq/L or 3.6 mEq/

75 membrane current for Pathway 2, perivascular potassium concentration for Pathway 3, and voltage-gated

76 ounterpart ([Formula: see text]), to monitor potassium concentration ([Formula: see text]) changes ([

77 The steady-state serum potassium concentration frequently changes during a card

78 eactions were slowed with an increase in the potassium concentration from 100 to 500 mM, via replacem

79 tamate inside the cell, raising the external potassium concentration generated an outward current att

80 A peak serum potassium concentration greater than 5.0 mmol/L develope

81 supplementing potassium to maintain a serum potassium concentration greater than or equal to 4.5 mEq

82 of patients; severe hyperkalemia (peak serum potassium concentration > or = 5.5 mmol/L) occurred in 2

83 may increase the risk of hyperkalemia (serum potassium concentration >5 mmol/L) in the setting of inc

84 s is mandated to avoid serious hyperkalemia (potassium concentration >5.5 mEq/L) and its attendant ri

85 tic, but the effect of such therapy on serum potassium concentration has not been established.

86 depolarized by ACh and by high extracellular potassium concentration (high K(+)).

87 ese fluctuations would abruptly alter plasma potassium concentration if not for rapid mechanisms, pri

88 cant role of P, S, and Mg in addition to the potassium concentration in determining the death interva

89 ect of increasing dietary potassium on serum potassium concentration in hypertensive individuals with

90 In conclusion, each drug increases plasma potassium concentration in patients with GS.

91 critical for the buffering of extracellular potassium concentration in retina.

92 ave attempted to screen charge by increasing potassium concentration in single-channel experiments.

93 method is suitable for estimating individual potassium concentration in small animals.

94 ecting intake, was estimated from sodium and potassium concentration in spot urine samples using the

95 tion between PK and U was independent of the potassium concentration in the bolus over the range of 2

96 Increased potassium concentration in the cleft maintained the hair

97 The serum potassium concentration in the control group was 4.33 +/

98 , a process necessary to maintain an optimal potassium concentration in the extracellular environment

99 he graphite (used as starting material), the potassium concentration in the intercalation compound, a

100 sugar, pH, conductivity, calcium, sodium and potassium concentration in the juice were also evaluated

101 lcium and sodium, but negatively affects the potassium concentration in the stele.

102 s in their calyx afferents by modulating the potassium concentration in the synaptic cleft, [K(+) ](c

103 A 10-fold decrease from the initial potassium concentration in the thin-layer solution was d

104 The serum potassium concentration in the treatment group (mean +/-

105 Low serum potassium concentrations in African Americans may contri

106 Whether interventions to increase serum potassium concentrations in African Americans might redu

107 Sodium and potassium concentrations in CSF were found higher in HS

108 this gap by varying nitrogen, magnesium, and potassium concentrations in hydroponically grown soybean

109 uggest that the measurement of intracellular potassium concentrations in red blood cells (RBC-K) can

110 that the presence of abnormal extracellular potassium concentrations in tumors suppresses the immune

111 f the GTP-FtsZ polymers decreased with lower potassium concentration, in contrast with the increase i

112 Extracellular potassium concentration increased during the cortical sp

113 Serum potassium concentration increased from 3.0 mmol/L to 4.3

114 On placebo therapy, the average serum potassium concentration increased slightly (0.4 mEq/L) d

115 Leaf nitrogen, phosphorus and potassium concentrations increased in response to the ad

116 g tetrad formation inside the cell where the potassium concentration is higher.

117 ensor for measuring extracellular changes in potassium concentration is selectivity against the compe

118 potassium intake is sensed, even when plasma potassium concentration is still within the normal range

119 vity filter of KcsA as a function of ambient potassium concentration is studied with solid-state NMR.

120 ng serum potassium (sK(+)) and hemodialysate potassium concentrations is uncertain.

121 l stage, but that depolarization by elevated potassium concentrations is without effect.

122 reversal potential was dependent on external potassium concentration; it was blocked by barium in the

123 ium (Kir) channels participate in regulating potassium concentration (K(+)) in the central nervous sy

124 pH (pH 2; H(3) PO(4) /KH(2) PO(4) ) and low potassium concentration ([K(+) ]=0.1 M) using organic fi

125 Extracellular potassium concentration ([K(+)](e)) is known to increase

126 e further enhanced by lowering extracellular potassium concentration ([K(+)](o)) from 5.4 to 3.6 mm.

127 is sensitive to changes in the extracellular potassium concentration ([K(+)](o)).

128 Blood potassium concentration ([K(+)]) influences the electroc

129 and Hazara virus (HAZV) exploit the changing potassium concentration ([K(+)]) of maturing endosomes t

130 Elevation of the extracellular potassium concentration ([K(+)]e) impairs T cell recepto

131 fects of depolarizing rises in extracellular potassium concentration ([K+](o)) on synapses, we depola

132 ar and extracellular pH evoked extracellular potassium concentration ([K+]o were recorded.

133 together with measurements of extracellular potassium concentration ([K+]o) and a transmural ECG.

134 The effects of raising extracellular potassium concentration ([K+]o) from 3.0 to 5.3, 9.5 or

135 ts such as I(Kr) or I(Kl) when extracellular potassium concentration ([K+]o) is increased.

136 In slice preparations, external potassium concentration ([K+]o) is typically elevated fr

137 essed by moderate rises in the extracellular potassium concentration ([K+]o).

138 During neuronal activity, extracellular potassium concentration ([K+]out) becomes elevated and,

139 nductance was dependent on the extracellular potassium concentration ([K]o).

140 tracellular) and erythrocyte (intracellular) potassium concentrations ([K+]e and [K+]i) were determin

141 n rapid renal responses to changes in plasma potassium concentration [K + ].

142 membrane depolarization induced by increased potassium concentration [K(+)] increased medium concentr

143 creases (0.5 to 2.0 mM) in the extracellular potassium concentration [K+]o.

144 s coincide with an increase in extracellular potassium concentrations [K(+)](e) yet little informatio

145 e is insensitive to changes in extracellular potassium concentration, [K+]o, because of the absence o

146 . Isolyte S 117 +/- 7 [p < .02]) and a lower potassium concentration (mEq/L: normal values 3.5 to 5.0

147 e exhibited less urinary flow, higher plasma potassium concentration, more fluid retention, and signi

148 e, mutant plants grew poorly on media with a potassium concentration of 100 micromolar or less.

149 eater than 150 mmol/L on admission; a plasma potassium concentration of less than 3.0 mmol/L on admis

150 r auditory hair cell function by maintaining potassium concentration of the scala media.

151 lemia as >=mild or >=moderate based on serum potassium concentrations of >5.5 or >6.0 mmol/L, respect

152 erkalemia as mild or moderate based on serum potassium concentrations of >5.5 or >6.0 mmol/L, respect

153 I) of incident diabetes for those with serum potassium concentrations of <4.0, 4.0-4.4, and 4.5-4.9 m

154 study, when clinically indicated, for serum potassium concentrations of 3.5 mmol/L or serum magnesiu

155 .5-4.9 mEq/L, compared with those with serum potassium concentrations of 5.0-5.5 mEq/L (referent), we

156 veground, with a particular increase in soil potassium concentration on day 15.

157 effect of light-evoked changes in subretinal potassium concentration on the transepithelial transport

158 the authors investigated the effects of high potassium concentrations on extracellular levels of gluc

159 with KGlu and was observed over an extended potassium concentration range.

160 the intake of healthy foods, whereas plasma potassium concentration remained stable within normal va

161 cluding plasma urea, creatinine, sodium, and potassium concentrations) remained within normal ranges

162 rrent was not altered by changes in external potassium concentration, replacing external cations with

163 thermore, maintaining a normal intracellular potassium concentration represses the cell death process

164 nd 0.001 for SBP and aldosterone and urinary potassium concentrations, respectively).

165 Potassium concentrations showed larger increases in sens

166 were associated with a slight rise in serum potassium concentrations (similar to placebo); this may

167 Plasma potassium concentration strongly and negatively correlat

168 detection of both conformers at low ambient potassium concentration suggests that the high-K(+) and

169 panediol linkers and its lower dependency on potassium concentration suggests that this complex conta

170 sis was detected by increasing extracellular potassium concentration to depolarize the oocyte membran

171 esponds rapidly and reversibly to changes in potassium concentrations typical of whole blood samples.

172 The measured potassium concentration (uncorrected for fat fraction) o

173 train lacking c-di-AMP is not viable at high potassium concentrations, unless the bacteria acquire su

174 in an increase in nitrogen, phosphorus, and potassium concentrations up to cycle 3 with maximum conc

175 ent temperatures and different extracellular potassium concentrations using the patch-clamp technique

176 s, by obtaining a linear optical response to potassium concentration via a simple, stackable design a

177 Baseline plasma potassium concentration was 2.8+/-0.4 mmol/L and increas

178 the combination group; the highest recorded potassium concentration was 5.8 mmol/L in a patient in t

179 f GTP, became larger and polydisperse as the potassium concentration was decreased.

180 The average potassium concentration was found to be significantly hi

181 elements, in wholemeal and white flour, but potassium concentration was higher in Rht-D1b lines.

182 ine transport was also assessed after apical potassium concentration was lowered from 6.0 to 2.2 mM t

183 Interstitial potassium concentration was regulated by both K+-pump an

184 applications of forskolin, dopamine, or high-potassium concentration, we image an increase in cAMP le

185 Fecal potassium output and serum potassium concentration were measured for 12 h.

186 However, OM, nitrogen, phosphorus and potassium concentration were significantly improved in t

187 ldosterone, urinary aldosterone, and urinary potassium concentrations were also significantly higher

188 Serum bicarbonate and potassium concentrations were drawn every 6 hrs for 72 h

189 Mean serum potassium concentrations were lower in African Americans

190 al potential differences and transepithelial potassium concentrations were measured in anaesthetized

191 11), whereas changes in serum phosphorus and potassium concentrations were not different from the pla

192 Leaf nitrogen and potassium concentrations were positively correlated with

193 d we review data linking serum and dialysate potassium concentrations with arrhythmias, cardiovascula

194 -h urinary potassium excretion [UKV; urinary potassium concentration x volume], the gold standard for