ライフサイエンスコーパス: lithium chloride

1 eta was abolished by the GSK3 beta inhibitor lithium chloride.

2 sucrose solution by pairing consumption with lithium chloride.

3 els by specific inhibition of GSK3beta using lithium chloride.

4 was paired with an injection of the emetic, lithium chloride.

5 ired with concurrent or delayed infusions of lithium chloride.

6 e suppressive effects of the aversive agent, lithium chloride.

7 e absence of PI3K signaling was induced with lithium chloride.

8 avor X alone was paired with the delivery of lithium chloride.

9 glycogen synthase kinase-3 (GSK-3) inhibitor lithium chloride.

10 ulators of Wnt activity, sodium butyrate and lithium chloride.

11 s the colonic lumen is readily accessible to lithium chloride.

12 Lithium chloride (0.15 mmol) was injected just downstrea

13 ed when given together with a single dose of lithium chloride (a nonselective GSK-3 inhibitor) or a p

14 atment in PbA-infected mice, the addition of lithium chloride, a compound which inhibits GSK3beta act

15 Finally, lithium chloride, a GSK3 inhibitor, also attenuated the

16 pidly, were protected from apoptosis by both lithium chloride, a GSK3 selective inhibitor, and inhibi

17 or the first time, the beneficial effects of lithium chloride, a reversible inhibitor of the glycogen

18 PE-specific gene expression was activated by lithium chloride, a Wnt/beta-catenin agonist.

19 hat flavor (satiation) or by pairing it with lithium chloride (acquired taste aversion), while the ot

20 Lithium chloride also increased osteoblast differentiati

21 Furthermore, in utero treatment with either lithium chloride, an agonist of canonical Wnt signaling,

22 s expressing wild type PS1 were treated with lithium chloride, an inhibitor of GSK-3beta.

23 Administration of GSK-3beta inhibitors lithium chloride and L803-mts restored glucose homeostas

24 es amylin and cholecystokinin, as well as by lithium chloride and lipopolysaccharide, compounds that

25 Molten mixtures of lithium chloride and metallic lithium are of significant

26 he physical chemistry of molten solutions of lithium chloride and metallic lithium, with and without

27 Paradoxically, the GSK3beta inhibitors lithium chloride and SB216763 selectively decreased the

28 Lithium chloride and SB216763, both glycogen synthase ki

29 scued from NVP-AEW541 by GSK3beta inhibitor, lithium chloride and were sensitized by GSK3beta activat

30 ss to sucrose and subsequently injected with lithium chloride, and a test phase in which animals were

31 uble factors (microRNA-206 inhibitor, IWR-1, Lithium Chloride, and BMP-4) (4F-AG-AMT).

32 ongly to stimuli such as potassium chloride, lithium chloride, and protein kinase C agonists.

33 ) inhibitors, especially the mood stabilizer lithium chloride, are also used as neuroprotective or an

34 showed both a conditioned place aversion to lithium chloride as well as CPP to palatable food.

35 echanical rotation, or late, by injection of lithium chloride (at 32 cells) or of the transcription f

36 the same effects in wild-type mice, whereas lithium chloride, at doses that produce conditioned tast

37 on, when GSK-3beta activity was inhibited by lithium chloride, both c-fos promoter activity and prote

38 orced expression of Wnt-1 and treatment with lithium chloride, both of which inhibit neural different

39 abrogated by nonspecific GSK3beta inhibitor lithium chloride but not by selective inhibitor SB216763

40 ly reflects cell survival, was maintained by lithium chloride, but not by caspase inhibition.

41 Furthermore, lithium chloride, but not caspase inhibition, prevented

42 ion is mediated by electronically stabilized lithium chloride carbenoids and affords a variety of dif

43 A, which encodes the cardiac sodium channel, lithium chloride caused concentration-dependent block of

44 ively regulated by AKT, using AR-A014418 and lithium chloride completely abolished LY294002-induced N

45 here also found to be opposite to those in a lithium chloride-conditioned avoidance task.

46 A lithium-chloride-containing hydrogel printing ink is dev

47 homologue of beta-catenin, although not in a lithium chloride-dependent manner.

48 We found that long-term exposure to lithium chloride dramatically protects cultured rat cere

49 Like illness-inducing agents (e.g., lithium chloride), drugs of abuse also suppress intake o

50 Conditioned taste aversions (CTA) based on lithium chloride (Experiment 1), amphetamine (Experiment

51 Feeding rats lithium chloride for 6 weeks, to produce a brain lithium

52 cyclic carbene (NHC) require the addition of lithium chloride for high levels of enantioselectivity.

53 Metalation with lithium-chloride-free LDA involves a rate-limiting deagg

54 of three steps: (1) loading the sorbent with lithium chloride from brine; (2) intermediate washing to

55 mn extraction process to selectively extract lithium chloride from geothermal brine.

56 o-T286 cyclin D1 expression was inhibited by lithium chloride, implicating GSK3 in these effects.

57 es were examined for the mechanistic role of lithium chloride in enabling this direct insertion.

58 Inhibition of Gsk3b using lithium chloride in Runx2-overexpressing osteoporotic fe

59 o blocked acquisition of ethanol-induced and lithium chloride-induced conditioned place aversion but

60 AC) that had previously been associated with lithium chloride-induced malaise, c-Fos protein expressi

61 aversion (CTA) for alanine when paired with lithium chloride-induced toxicosis.

62 r flavors paired with toxic drug treatments (lithium chloride infusion or methylscopolamine injection

63 Lithium chloride inhibition of GSK-3beta increased nucle

64 curves were recorded following injection of lithium chloride into the right or left atrium.

65 ed ions; (3) final washing for unloading the lithium chloride ions.

66 mation and suspension of lithium clusters in lithium chloride is the cause of various phenomena exhib

67 iodides with indium metal in the presence of lithium chloride leads to the formation of an organoindi

68 urately by using central venous injection of lithium chloride (Li-CCO).

69 by using peripheral venous administration of lithium chloride (Li-PCO) with Li-CCO.

70 When lithium chloride (LiCI) was used as the US, AP-lesioned

71 Lithium chloride (LiCl(2)) 3.0mEq/kg IP acutely lowered

72 s of C57BL/6J fetal mice pretreated with E2, lithium chloride (LiCl) and combined E2/LiCl for 12, 24

73 oral effects of short-term administration of lithium chloride (LiCl) and valproic acid (VPA) in rats.

74 ontaining WNT3A or the WNT pathway activator lithium chloride (LiCl) display accelerated formation of

75 Lithium chloride (LiCl) exhibits significant therapeutic

76 0.3% oral saccharin (SAC) and 81 mg/kg i.p. lithium chloride (LiCl) followed by extinction training

77 Acute injection of a high dose of lithium chloride (LiCl) increases c-Fos expression in th

78 n their home cages immediately followed by a lithium chloride (LiCl) injection on 3 consecutive days.

79 eck a bead presented 15 or more min before a lithium chloride (LiCl) injection, but would peck a bead

80 that N,N-dimethylacetamide (DMA) containing lithium chloride (LiCl) is a privileged solvent that ena

81 hen it is paired with an aversive agent like lithium chloride (LiCl) or a preferred substance such as

82 P-1) and intraperitoneal (i.p.) injection of lithium chloride (LiCl) produce similar patterns of c-Fo

83 ulocyte-colony stimulating factor (G-CSF) or lithium chloride (LiCl) produced synergistic terminal di

84 Peripheral administration of large doses of lithium chloride (LiCl) to rats causes a spectrum of eff

85 conditioned taste aversion (CTA) induced by lithium chloride (LiCl) toxicosis (Experiments 1 and 4).

86 failed to learn a taste aversion induced by lithium chloride (LiCl) toxicosis.

87 Lithium chloride (LiCl) treatment activated Wnt signalin

88 of appetite-suppressing substances including lithium chloride (LiCl), a compound often used to induce

89 Additionally, exogenous compounds, such as lithium chloride (LiCl), a salt that creates gastric dis

90 Lithium chloride (LiCl), an inhibitor of glycogen syntha

91 ointestinal (GI) infusion of 1 nutrient with lithium chloride (LiCl), whereas they could not discrimi

92 Similar results were obtained with lithium chloride (LiCl), which does not affect protein s

93 ation on subsequent acquisition of EtOH- and lithium chloride (LiCl)-induced conditioned taste aversi

94 orphine treatment on cocaine-, sucrose-, and lithium chloride (LiCl)-induced suppression of saccharin

95 IN2 siRNA reduces inhibitory GSK3 levels and lithium chloride (LiCl)-upregulated beta-catenin or CCAA

96 igated here using the malaise-inducing agent lithium chloride (LiCl).

97 husk, with different added concentrations of lithium chloride (LiCl).

98 h was attenuated by LY294002 and enhanced by lithium chloride (LiCl).

99 acological stimulation of Wnt signaling with lithium chloride (LiCl).

100 ered intraperitoneal injections of saline or lithium chloride (LiCl; .15 M) following exposure to a n

101 ral saccharin (SAC; the CS) and 81mg/kg i.p. lithium chloride (LiCl; the US)] followed by extinction

102 charin, SAC) and unconditioned stimulus (US; lithium chloride, LiCl).

103 acetaldehyde (lithium vinyloxide, LiOV) and lithium chloride, lithium bromide, and lithium amides.

104 Lithium chloride markedly enhanced Cre-Lox-mediated Wnt-

105 In addition, lithium chloride-mediated inhibition of GSK3beta also re

106 expression of constitutively active AKT and lithium chloride-mediated inhibition of GSK3beta reduce

107 dard saccharin CS paired with the following: lithium chloride, morphine, amphetamine, or sucrose.

108 y, treatment with the autophagic stimulators lithium chloride or rapamycin reverses the bioenergetic

109 promoter (hAPP tg) were treated with either lithium chloride or saline alone.

110 mutant beta-catenin, treatment of cells with lithium chloride, or with wnt3a-conditioned medium, thre

111 le research has been done on its role in the lithium chloride-pilocarpine induced epileptic model.

112 e Sprague Dawley (SD) rats were treated with lithium chloride-pilocarpine injections and divided into

113 plar MS system used for characterization was lithium chloride/potassium chloride eutectic (LKE), whic

114 cking it using a dominant-negative mutant or lithium chloride prevented mTORC1-induced accelerated ax

115 Inhibition of GSK3 by lithium chloride reduced its association with TSC1 where

116 administration of an aversive agent such as lithium chloride (referred to as a conditioned taste ave

117 slation by cycloheximide, or of autophagy by lithium chloride, rescued viability, preserved cellular

118 intraperitoneal administration of the toxin lithium chloride resulted in a diminished CTA.

119 n D1 is inhibited by the GSK3beta inhibitors lithium chloride, SB216763, and SB415286.

120 Embryos cultured in 400 mM lithium chloride sea water showed marked delay to the ce

121 ctivity using either a specific inhibitor or lithium chloride significantly reduced tau phosphorylati

122 Transmetalation with zinc chloride then (lithium chloride solubilized) copper cyanide followed by

123 The data are consistent with lithium chloride solubilizing organozinc reagents from t

124 oncentrations, and apply our method to study lithium chloride solutions at concentrations >0.5 M.

125 he glycogen synthase kinase-3 beta inhibitor lithium chloride suppressed the glycogen synthase kinase

126 high selectivity, whereas in the presence of lithium chloride the syn adduct is favored.

127 brain areas consequent to administration of lithium chloride, the typical illness-inducing agent use

128 Aged MSCs treated with lithium chloride-to increase the bioavailability of beta

129 ngly with degree of axonal degeneration, and lithium-chloride-treated mice showed less degeneration i

130 Following lithium chloride treatment (10 mg/kg, s.c.), (R/S)-3, 5-

131 increased basal beta-catenin levels, such as lithium chloride treatment or repression of caveolin-1 e

132 activation of Wnt/beta-catenin signaling by lithium chloride treatment reduced the number and activi

133 Interestingly, lithium chloride treatment was able to suppress the gain

134 First, dorsalization by lithium chloride treatment was completely blocked by Chd

135 egenerating dorsal and ventral half-embryos, lithium chloride treatment, and the overexpression of Wn

136 controls received either saline or unpaired lithium chloride treatment.

137 ween an olfactory conditioned stimulus and a lithium chloride unconditioned stimulus.

138 Treatment of cells with a Wnt activator, lithium chloride, up-regulated DPAGT1 transcript levels

139 Activation of Wnt signaling using lithium chloride was achieved in vitro and its effects o

140 Using the specific GSK3 inhibitor lithium chloride, we have provided strong circumstantial

141 tablished in golden hamsters by injection of lithium chloride, were quantified as percent suppression

142 oderm-specific genes can be induced by 25 mM lithium chloride, which also induced endoderm formation.

143 Lithium chloride, which enhances the accumulation of bet

144 The IC50 for glycogen synthase peptide and lithium chloride, which has been reported to be uncompet

145 Conversely, lithium chloride, which inhibits glycogen synthase kinas

146 lial cells; activation of Wnt signaling with lithium chloride, which stabilizes beta-catenin levels,