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1 ulators of Wnt activity, sodium butyrate and lithium chloride.
2 s the colonic lumen is readily accessible to lithium chloride.
3 eta was abolished by the GSK3 beta inhibitor lithium chloride.
4 sucrose solution by pairing consumption with lithium chloride.
5 els by specific inhibition of GSK3beta using lithium chloride.
6  was paired with an injection of the emetic, lithium chloride.
7 ired with concurrent or delayed infusions of lithium chloride.
8 e suppressive effects of the aversive agent, lithium chloride.
9  catalysis is required for chlorination with lithium chloride.
10 e absence of PI3K signaling was induced with lithium chloride.
11 avor X alone was paired with the delivery of lithium chloride.
12 glycogen synthase kinase-3 (GSK-3) inhibitor lithium chloride.
13                                              Lithium chloride (0.15 mmol) was injected just downstrea
14 ed when given together with a single dose of lithium chloride (a nonselective GSK-3 inhibitor) or a p
15 atment in PbA-infected mice, the addition of lithium chloride, a compound which inhibits GSK3beta act
16                                     Finally, lithium chloride, a GSK3 inhibitor, also attenuated the
17 pidly, were protected from apoptosis by both lithium chloride, a GSK3 selective inhibitor, and inhibi
18 or the first time, the beneficial effects of lithium chloride, a reversible inhibitor of the glycogen
19 PE-specific gene expression was activated by lithium chloride, a Wnt/beta-catenin agonist.
20 hat flavor (satiation) or by pairing it with lithium chloride (acquired taste aversion), while the ot
21                                              Lithium chloride also increased osteoblast differentiati
22  Furthermore, in utero treatment with either lithium chloride, an agonist of canonical Wnt signaling,
23 s expressing wild type PS1 were treated with lithium chloride, an inhibitor of GSK-3beta.
24 le-stranded RNA was precipitated using 4.0 M Lithium Chloride and centrifugation.
25       Administration of GSK-3beta inhibitors lithium chloride and L803-mts restored glucose homeostas
26 es amylin and cholecystokinin, as well as by lithium chloride and lipopolysaccharide, compounds that
27                           Molten mixtures of lithium chloride and metallic lithium are of significant
28 he physical chemistry of molten solutions of lithium chloride and metallic lithium, with and without
29       Paradoxically, the GSK3beta inhibitors lithium chloride and SB216763 selectively decreased the
30                                              Lithium chloride and SB216763, both glycogen synthase ki
31 scued from NVP-AEW541 by GSK3beta inhibitor, lithium chloride and were sensitized by GSK3beta activat
32 ss to sucrose and subsequently injected with lithium chloride, and a test phase in which animals were
33 uble factors (microRNA-206 inhibitor, IWR-1, Lithium Chloride, and BMP-4) (4F-AG-AMT).
34 ongly to stimuli such as potassium chloride, lithium chloride, and protein kinase C agonists.
35 ) inhibitors, especially the mood stabilizer lithium chloride, are also used as neuroprotective or an
36  showed both a conditioned place aversion to lithium chloride as well as CPP to palatable food.
37 echanical rotation, or late, by injection of lithium chloride (at 32 cells) or of the transcription f
38  the same effects in wild-type mice, whereas lithium chloride, at doses that produce conditioned tast
39 on, when GSK-3beta activity was inhibited by lithium chloride, both c-fos promoter activity and prote
40 orced expression of Wnt-1 and treatment with lithium chloride, both of which inhibit neural different
41  abrogated by nonspecific GSK3beta inhibitor lithium chloride but not by selective inhibitor SB216763
42 ly reflects cell survival, was maintained by lithium chloride, but not by caspase inhibition.
43                                 Furthermore, lithium chloride, but not caspase inhibition, prevented
44 ion is mediated by electronically stabilized lithium chloride carbenoids and affords a variety of dif
45 A, which encodes the cardiac sodium channel, lithium chloride caused concentration-dependent block of
46 ively regulated by AKT, using AR-A014418 and lithium chloride completely abolished LY294002-induced N
47 here also found to be opposite to those in a lithium chloride-conditioned avoidance task.
48                                            A lithium-chloride-containing hydrogel printing ink is dev
49 homologue of beta-catenin, although not in a lithium chloride-dependent manner.
50          We found that long-term exposure to lithium chloride dramatically protects cultured rat cere
51          Like illness-inducing agents (e.g., lithium chloride), drugs of abuse also suppress intake o
52 dress this issue by employing a concentrated lithium chloride electrolyte, which stabilizes reactive
53   Conditioned taste aversions (CTA) based on lithium chloride (Experiment 1), amphetamine (Experiment
54           Disruption of G4-RNA structures by lithium chloride failed to bind with FXR1, indicating it
55                                 Feeding rats lithium chloride for 6 weeks, to produce a brain lithium
56 cyclic carbene (NHC) require the addition of lithium chloride for high levels of enantioselectivity.
57                              Metalation with lithium-chloride-free LDA involves a rate-limiting deagg
58 of three steps: (1) loading the sorbent with lithium chloride from brine; (2) intermediate washing to
59 mn extraction process to selectively extract lithium chloride from geothermal brine.
60 eding behaviour of peptide YY3-36 (PYY3-36), lithium chloride, glucagon-like peptide 1 (GLP-1), and l
61        Structural and rate studies show that lithium chloride has little effect on the dynamics of th
62 o-T286 cyclin D1 expression was inhibited by lithium chloride, implicating GSK3 in these effects.
63 es were examined for the mechanistic role of lithium chloride in enabling this direct insertion.
64 l, MgCl(2), and CaCl(2) and then release the lithium chloride in methanol.
65                                We pinpointed lithium chloride in mTeSR1 as a cause of XIST RNA loss.
66                    Inhibition of Gsk3b using lithium chloride in Runx2-overexpressing osteoporotic fe
67 o blocked acquisition of ethanol-induced and lithium chloride-induced conditioned place aversion but
68 both WT and DAT-Ala53 mice exhibited similar lithium chloride-induced CPA and morphine-induced CPP.
69 AC) that had previously been associated with lithium chloride-induced malaise, c-Fos protein expressi
70  aversion (CTA) for alanine when paired with lithium chloride-induced toxicosis.
71 r flavors paired with toxic drug treatments (lithium chloride infusion or methylscopolamine injection
72                                              Lithium chloride inhibition of GSK-3beta increased nucle
73  curves were recorded following injection of lithium chloride into the right or left atrium.
74 ed ions; (3) final washing for unloading the lithium chloride ions.
75                                              Lithium chloride is known to promote the direct insertio
76 mation and suspension of lithium clusters in lithium chloride is the cause of various phenomena exhib
77 lyte reduction to sulfur, sulfur dioxide and lithium chloride, is well known for its high energy dens
78 iodides with indium metal in the presence of lithium chloride leads to the formation of an organoindi
79 urately by using central venous injection of lithium chloride (Li-CCO).
80 by using peripheral venous administration of lithium chloride (Li-PCO) with Li-CCO.
81                                         When lithium chloride (LiCI) was used as the US, AP-lesioned
82                                              Lithium chloride (LiCl(2)) 3.0mEq/kg IP acutely lowered
83 s of C57BL/6J fetal mice pretreated with E2, lithium chloride (LiCl) and combined E2/LiCl for 12, 24
84  followed by an intraperitoneal injection of lithium chloride (LiCl) and served to pair the memory of
85 oral effects of short-term administration of lithium chloride (LiCl) and valproic acid (VPA) in rats.
86                              By adding 50 mM lithium chloride (LiCl) as an electrolyte additive, we s
87 raoral sucrose with malaise via injection of lithium chloride (LiCl) caused the development of a cond
88 ontaining WNT3A or the WNT pathway activator lithium chloride (LiCl) display accelerated formation of
89                                              Lithium chloride (LiCl) exhibits significant therapeutic
90  0.3% oral saccharin (SAC) and 81 mg/kg i.p. lithium chloride (LiCl) followed by extinction training
91 d the dorsalizing effects of the Wnt agonist lithium chloride (LiCl) in embryos, and this effect requ
92            Acute injection of a high dose of lithium chloride (LiCl) increases c-Fos expression in th
93 n their home cages immediately followed by a lithium chloride (LiCl) injection on 3 consecutive days.
94 eck a bead presented 15 or more min before a lithium chloride (LiCl) injection, but would peck a bead
95  that N,N-dimethylacetamide (DMA) containing lithium chloride (LiCl) is a privileged solvent that ena
96 -catenin knockdown embryos, dorsalization by Lithium chloride (LiCl) is mediated by Nodals, Dkk1 exer
97 hen it is paired with an aversive agent like lithium chloride (LiCl) or a preferred substance such as
98 P-1) and intraperitoneal (i.p.) injection of lithium chloride (LiCl) produce similar patterns of c-Fo
99 ulocyte-colony stimulating factor (G-CSF) or lithium chloride (LiCl) produced synergistic terminal di
100                   We report that addition of lithium chloride (LiCl) to PDF is a translatable interve
101  Peripheral administration of large doses of lithium chloride (LiCl) to rats causes a spectrum of eff
102  conditioned taste aversion (CTA) induced by lithium chloride (LiCl) toxicosis (Experiments 1 and 4).
103  failed to learn a taste aversion induced by lithium chloride (LiCl) toxicosis.
104                                              Lithium chloride (LiCl) treatment activated Wnt signalin
105 in and Col1a1 expression can be increased by lithium chloride (LiCl) treatment in the in vitro tooth
106 ogen synthase kinase 3 (GSK3) inhibition via lithium chloride (LiCl) treatment on SERCA uncoupling in
107 of appetite-suppressing substances including lithium chloride (LiCl), a compound often used to induce
108          The current study hypothesizes that lithium chloride (LiCl), a potent activator of the Wnt/B
109   Additionally, exogenous compounds, such as lithium chloride (LiCl), a salt that creates gastric dis
110                                              Lithium chloride (LiCl), an inhibitor of glycogen syntha
111 ointestinal (GI) infusion of 1 nutrient with lithium chloride (LiCl), whereas they could not discrimi
112           Similar results were obtained with lithium chloride (LiCl), which does not affect protein s
113 ation on subsequent acquisition of EtOH- and lithium chloride (LiCl)-induced conditioned taste aversi
114 orphine treatment on cocaine-, sucrose-, and lithium chloride (LiCl)-induced suppression of saccharin
115 IN2 siRNA reduces inhibitory GSK3 levels and lithium chloride (LiCl)-upregulated beta-catenin or CCAA
116 igated here using the malaise-inducing agent lithium chloride (LiCl).
117 husk, with different added concentrations of lithium chloride (LiCl).
118 h was attenuated by LY294002 and enhanced by lithium chloride (LiCl).
119 acological stimulation of Wnt signaling with lithium chloride (LiCl).
120 ered intraperitoneal injections of saline or lithium chloride (LiCl; .15 M) following exposure to a n
121 ral saccharin (SAC; the CS) and 81mg/kg i.p. lithium chloride (LiCl; the US)] followed by extinction
122 charin, SAC) and unconditioned stimulus (US; lithium chloride, LiCl).
123  and chemical resolution of the interface of lithium chloride - lithium bis(trifluoromethanesulfonyl)
124  acetaldehyde (lithium vinyloxide, LiOV) and lithium chloride, lithium bromide, and lithium amides.
125                                              Lithium chloride markedly enhanced Cre-Lox-mediated Wnt-
126                                 In addition, lithium chloride-mediated inhibition of GSK3beta also re
127  expression of constitutively active AKT and lithium chloride-mediated inhibition of GSK3beta reduce
128 dard saccharin CS paired with the following: lithium chloride, morphine, amphetamine, or sucrose.
129          We exposed cultures for one week to lithium chloride or distilled water, extracted total RNA
130                              The addition of lithium chloride or inhibitors of GSK-3 proteins that ar
131 y, treatment with the autophagic stimulators lithium chloride or rapamycin reverses the bioenergetic
132  promoter (hAPP tg) were treated with either lithium chloride or saline alone.
133 mutant beta-catenin, treatment of cells with lithium chloride, or with wnt3a-conditioned medium, thre
134 le research has been done on its role in the lithium chloride-pilocarpine induced epileptic model.
135 e Sprague Dawley (SD) rats were treated with lithium chloride-pilocarpine injections and divided into
136 plar MS system used for characterization was lithium chloride/potassium chloride eutectic (LKE), whic
137          These two gels were found to adsorb lithium chloride preferentially from an acetonitrile sol
138 cking it using a dominant-negative mutant or lithium chloride prevented mTORC1-induced accelerated ax
139                                              Lithium chloride prevented the expansion of Apc-mutant c
140                        Inhibition of GSK3 by lithium chloride reduced its association with TSC1 where
141  administration of an aversive agent such as lithium chloride (referred to as a conditioned taste ave
142 slation by cycloheximide, or of autophagy by lithium chloride, rescued viability, preserved cellular
143  intraperitoneal administration of the toxin lithium chloride resulted in a diminished CTA.
144 n D1 is inhibited by the GSK3beta inhibitors lithium chloride, SB216763, and SB415286.
145                   Embryos cultured in 400 mM lithium chloride sea water showed marked delay to the ce
146 ctivity using either a specific inhibitor or lithium chloride significantly reduced tau phosphorylati
147     Transmetalation with zinc chloride then (lithium chloride solubilized) copper cyanide followed by
148                 The data are consistent with lithium chloride solubilizing organozinc reagents from t
149 ater-water H-bonding present in concentrated lithium chloride solutions (up to four waters per ion pa
150 oncentrations, and apply our method to study lithium chloride solutions at concentrations >0.5 M.
151 he glycogen synthase kinase-3 beta inhibitor lithium chloride suppressed the glycogen synthase kinase
152 high selectivity, whereas in the presence of lithium chloride the syn adduct is favored.
153  brain areas consequent to administration of lithium chloride, the typical illness-inducing agent use
154 sinibacillus sphaericus biomineralization of lithium chloride to lithium hydroxide.
155                       Aged MSCs treated with lithium chloride-to increase the bioavailability of beta
156 ngly with degree of axonal degeneration, and lithium-chloride-treated mice showed less degeneration i
157                                    Following lithium chloride treatment (10 mg/kg, s.c.), (R/S)-3, 5-
158 increased basal beta-catenin levels, such as lithium chloride treatment or repression of caveolin-1 e
159  activation of Wnt/beta-catenin signaling by lithium chloride treatment reduced the number and activi
160                               Interestingly, lithium chloride treatment was able to suppress the gain
161                      First, dorsalization by lithium chloride treatment was completely blocked by Chd
162 egenerating dorsal and ventral half-embryos, lithium chloride treatment, and the overexpression of Wn
163  controls received either saline or unpaired lithium chloride treatment.
164 ween an olfactory conditioned stimulus and a lithium chloride unconditioned stimulus.
165     Treatment of cells with a Wnt activator, lithium chloride, up-regulated DPAGT1 transcript levels
166 ton Sea geothermal brine and purification of lithium chloride using intercalation materials, and conv
167            Activation of Wnt signaling using lithium chloride was achieved in vitro and its effects o
168            Using the specific GSK3 inhibitor lithium chloride, we have provided strong circumstantial
169 tablished in golden hamsters by injection of lithium chloride, were quantified as percent suppression
170 oderm-specific genes can be induced by 25 mM lithium chloride, which also induced endoderm formation.
171                                              Lithium chloride, which enhances the accumulation of bet
172   The IC50 for glycogen synthase peptide and lithium chloride, which has been reported to be uncompet
173                                  Conversely, lithium chloride, which inhibits glycogen synthase kinas
174 lial cells; activation of Wnt signaling with lithium chloride, which stabilizes beta-catenin levels,

 
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