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Disruption of contact inhibition, which was induced by toxic AhR ligands 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or << polycyclic aromatic hydrocarbons >> in epithelial WB-F344 cells, reduced [[ Cx43 ]] protein levels, possibly via enhanced proteasomal degradation, significantly decreased the amount of gap junction plaques and downregulated GJIC, in an AhR-dependent manner.

Although both intracellular and membrane Cx43 pools were markedly reduced in cells released from contact inhibition by << TCDD >>, siRNA-mediated [[ Cx43 ]] knock-down was not sufficient to stimulate proliferation in contact-inhibited cells.

Although both intracellular and membrane << Cx43 >> pools were markedly reduced in cells released from contact inhibition by [[ TCDD ]], siRNA-mediated Cx43 knock-down was not sufficient to stimulate proliferation in contact-inhibited cells.

<< Dexamethasone >> suppresses histamine synthesis by repressing both transcription and activity of [[ HDC ]] in allergic rats.

<< Dexamethasone >> suppresses histamine synthesis by repressing both transcription and activity of [[ HDC ]] in allergic rats.

BACKGROUND: << Histamine >> synthesized by [[ histidine decarboxylase ]] (HDC) from L-histidine is a major chemical mediator in the development of nasal allergy which is characterized by nasal hypersensitivity.

BACKGROUND: << Histamine >> synthesized by histidine decarboxylase ([[ HDC ]]) from L-histidine is a major chemical mediator in the development of nasal allergy which is characterized by nasal hypersensitivity.

BACKGROUND: Histamine synthesized by << histidine decarboxylase >> (HDC) from [[ L-histidine ]] is a major chemical mediator in the development of nasal allergy which is characterized by nasal hypersensitivity.

BACKGROUND: Histamine synthesized by histidine decarboxylase (<< HDC >>) from [[ L-histidine ]] is a major chemical mediator in the development of nasal allergy which is characterized by nasal hypersensitivity.

However the regulatory mechanism of << histamine >> synthesis by [[ HDC ]] remains to be elucidated.

Histamine content, << HDC >> activity and HDC mRNA expression in nasal mucosa were also significantly increased after [[ TDI ]] provocation.

Histamine content, HDC activity and << HDC >> mRNA expression in nasal mucosa were also significantly increased after [[ TDI ]] provocation.

Pretreatment with dexamethasone significantly suppressed nasal allergy-like behaviors, up-regulation of histamine content, << HDC >> activity and HDC mRNA induced by [[ TDI ]] in TDI-sensitized rats.

Pretreatment with dexamethasone significantly suppressed nasal allergy-like behaviors, up-regulation of histamine content, HDC activity and << HDC >> mRNA induced by [[ TDI ]] in TDI-sensitized rats.

Pretreatment with dexamethasone significantly suppressed nasal allergy-like behaviors, up-regulation of histamine content, HDC activity and << HDC >> mRNA induced by TDI in [[ TDI ]]-sensitized rats.

Pretreatment with << dexamethasone >> significantly suppressed nasal allergy-like behaviors, up-regulation of histamine content, HDC activity and [[ HDC ]] mRNA induced by TDI in TDI-sensitized rats.

Pretreatment with << dexamethasone >> significantly suppressed nasal allergy-like behaviors, up-regulation of histamine content, [[ HDC ]] activity and HDC mRNA induced by TDI in TDI-sensitized rats.

CONCLUSIONS: These findings indicate that increased synthesis of << histamine >> through up-regulation of [[ HDC ]] gene expression and HDC activity in nasal mucosa plays an important role in the development of nasal hypersensitivity.

CONCLUSIONS: These findings indicate that increased synthesis of << histamine >> through up-regulation of HDC gene expression and [[ HDC ]] activity in nasal mucosa plays an important role in the development of nasal hypersensitivity.

Repression of << HDC >> gene expression and HDC activity by [[ dexamethasone ]] may underlie its therapeutic effect in the treatment of allergy.

Repression of HDC gene expression and << HDC >> activity by [[ dexamethasone ]] may underlie its therapeutic effect in the treatment of allergy.

CONCLUSIONS A diet that partially replaces << carbohydrate >> with unsaturated fat may improve [[ insulin ]] sensitivity in a population at risk for cardiovascular disease.

In this study, we assessed the effects of << clopidogrel >> and clarithromycin, known CYP2B6 and CYP3A inhibitors, respectively, on the enantioselective disposition of racemic sibutramine in conjunction with [[ CYP2B6 ]] polymorphisms in humans.

In this study, we assessed the effects of << clopidogrel >> and clarithromycin, known [[ CYP2B6 ]] and CYP3A inhibitors, respectively, on the enantioselective disposition of racemic sibutramine in conjunction with CYP2B6 polymorphisms in humans.

In this study, we assessed the effects of << clopidogrel >> and clarithromycin, known CYP2B6 and [[ CYP3A ]] inhibitors, respectively, on the enantioselective disposition of racemic sibutramine in conjunction with CYP2B6 polymorphisms in humans.

In this study, we assessed the effects of clopidogrel and << clarithromycin >>, known [[ CYP2B6 ]] and CYP3A inhibitors, respectively, on the enantioselective disposition of racemic sibutramine in conjunction with CYP2B6 polymorphisms in humans.

In this study, we assessed the effects of clopidogrel and << clarithromycin >>, known CYP2B6 and [[ CYP3A ]] inhibitors, respectively, on the enantioselective disposition of racemic sibutramine in conjunction with CYP2B6 polymorphisms in humans.

Increased << IL-5 >> activity in the serum was inhibited by both [[ pranlukast ]] and MCI-826 by over 90%.

Increased << IL-5 >> activity in the serum was inhibited by both pranlukast and [[ MCI-826 ]] by over 90%.

CONCLUSIONS: << CysLTs >> produced after antigen provocation sequentially induced IL-5 production from some immune component cells via [[ CysLT1 ]] receptor activation.

Extracellular application of meclofenamate (EC(50) = 25 microM) and << diclofenac >> (EC(50) = 2.6 microM) resulted in the activation of [[ KCNQ2/Q3 ]] K(+) currents, heterologously expressed in Chinese hamster ovary cells.

Extracellular application of << meclofenamate >> (EC(50) = 25 microM) and diclofenac (EC(50) = 2.6 microM) resulted in the activation of [[ KCNQ2/Q3 ]] K(+) currents, heterologously expressed in Chinese hamster ovary cells.

The selective << norepinephrine (NE) transporter >> inhibitor [[ atomoxetine ]] (formerly called tomoxetine or LY139603) has been shown to alleviate symptoms in Attention Deficit/Hyperactivity Disorder (ADHD).

The selective << norepinephrine (NE) transporter >> inhibitor atomoxetine (formerly called [[ tomoxetine ]] or LY139603) has been shown to alleviate symptoms in Attention Deficit/Hyperactivity Disorder (ADHD).

The selective << norepinephrine (NE) transporter >> inhibitor atomoxetine (formerly called tomoxetine or [[ LY139603 ]]) has been shown to alleviate symptoms in Attention Deficit/Hyperactivity Disorder (ADHD).

Lung inflammation, << IL-4 >> production, and airway mast cell activity were also prevented under this early short-term treatment with [[ PGE2 ]].

Local << PGE2 >> administration prevented the increase of airway [[ IL-13 ]] and osteopontin and kept lung plasmacytoid dendritic cell counts close to baseline.

Local << PGE2 >> administration prevented the increase of airway IL-13 and [[ osteopontin ]] and kept lung plasmacytoid dendritic cell counts close to baseline.

Reactivators showed different activity in the reactivation of << rat brain AChE >> after [[ dichlorvos ]], paraoxon and tabun inhibition.

Reactivators showed different activity in the reactivation of << rat brain AChE >> after dichlorvos, [[ paraoxon ]] and tabun inhibition.

Reactivators showed different activity in the reactivation of << rat brain AChE >> after dichlorvos, paraoxon and [[ tabun ]] inhibition.

<< AChE >> was easier reactivated after [[ paraoxon ]] treatment.

The reactivation of brain << AChE >> inhibited with tabun demonstrated better activity of new compound [[ BT-07-4M ]], TMB-4 and obidoxime from symmetric oximes, and BT-05 and BT-03 possessing asymmetric structure.

The reactivation of brain << AChE >> inhibited with tabun demonstrated better activity of new compound BT-07-4M, [[ TMB-4 ]] and obidoxime from symmetric oximes, and BT-05 and BT-03 possessing asymmetric structure.

The reactivation of brain << AChE >> inhibited with tabun demonstrated better activity of new compound BT-07-4M, TMB-4 and [[ obidoxime ]] from symmetric oximes, and BT-05 and BT-03 possessing asymmetric structure.

The reactivation of brain << AChE >> inhibited with tabun demonstrated better activity of new compound BT-07-4M, TMB-4 and obidoxime from symmetric [[ oximes ]], and BT-05 and BT-03 possessing asymmetric structure.

The reactivation of brain << AChE >> inhibited with tabun demonstrated better activity of new compound BT-07-4M, TMB-4 and obidoxime from symmetric oximes, and [[ BT-05 ]] and BT-03 possessing asymmetric structure.

The reactivation of brain << AChE >> inhibited with tabun demonstrated better activity of new compound BT-07-4M, TMB-4 and obidoxime from symmetric oximes, and BT-05 and [[ BT-03 ]] possessing asymmetric structure.

All compounds showed low activity toward inhibition of << AChE >> caused by [[ dichlorvos ]].

State-dependent << mibefradil >> block of [[ Na+ channels ]].

<< Mibefradil >> is a [[ T-type Ca2+ channel ]] antagonist with reported cross-reactivity with other classes of ion channels, including K+, Cl-, and Na+ channels.

Using whole-cell voltage clamp, we examined << mibefradil >> block of four [[ Na+ channel ]] isoforms expressed in human embryonic kidney cells: Nav1.5 (cardiac), Nav1.4 (skeletal muscle), Nav1.2 (brain), and Nav1.7 (peripheral nerve).

Using whole-cell voltage clamp, we examined << mibefradil >> block of four Na+ channel isoforms expressed in human embryonic kidney cells: [[ Nav1.5 ]] (cardiac), Nav1.4 (skeletal muscle), Nav1.2 (brain), and Nav1.7 (peripheral nerve).

Using whole-cell voltage clamp, we examined << mibefradil >> block of four Na+ channel isoforms expressed in human embryonic kidney cells: Nav1.5 (cardiac), [[ Nav1.4 ]] (skeletal muscle), Nav1.2 (brain), and Nav1.7 (peripheral nerve).

Using whole-cell voltage clamp, we examined << mibefradil >> block of four Na+ channel isoforms expressed in human embryonic kidney cells: Nav1.5 (cardiac), Nav1.4 (skeletal muscle), [[ Nav1.2 ]] (brain), and Nav1.7 (peripheral nerve).

Using whole-cell voltage clamp, we examined << mibefradil >> block of four Na+ channel isoforms expressed in human embryonic kidney cells: Nav1.5 (cardiac), Nav1.4 (skeletal muscle), Nav1.2 (brain), and [[ Nav1.7 ]] (peripheral nerve).

<< Mibefradil >> blocked [[ Nav1.5 ]] in a use/frequency-dependent manner, indicating preferential binding to states visited during depolarization.

<< Mibefradil >> blocked currents of all [[ Na+ channel ]] isoforms with similar affinity and a dependence on holding potential, and drug off-rate was slowed at depolarized potentials (k(off) was 0.024/s at -130 mV and 0.007/s at -100 mV for Nav1.5).

<< Mibefradil >> blocked currents of all Na+ channel isoforms with similar affinity and a dependence on holding potential, and drug off-rate was slowed at depolarized potentials (k(off) was 0.024/s at -130 mV and 0.007/s at -100 mV for [[ Nav1.5 ]]).

In addition, inhibiting the binding of the fast inactivation lid (<< Nav1.5 >> ICM + MTSET) did not alter [[ mibefradil ]] block, confirming that the drug does not preferentially interact with the fast-inactivated state.

When selectively applied to channels after inducing slow inactivation with a 60-s pulse to -10 mV, << mibefradil >> (1 microM) produced 45% fractional block in [[ Nav1.5 ]] and greater block (88%) in an isoform (Nav1.4) that slow-inactivates more completely.

When selectively applied to channels after inducing slow inactivation with a 60-s pulse to -10 mV, << mibefradil >> (1 microM) produced 45% fractional block in Nav1.5 and greater block (88%) in an isoform ([[ Nav1.4 ]]) that slow-inactivates more completely.

Our results suggest that << mibefradil >> blocks [[ Na+ channels ]] in a state-dependent manner that does not depend on fast inactivation but probably involves interaction with one or more slow-inactivated state(s).

<< Docetaxel >> is a semisynthetic taxane that inhibit tumor growth by induction of microtubule stabilization and promotion of [[ bcl-2 ]] inactivation, which induce apoptosis.

Docetaxel is a semisynthetic << taxane >> that inhibit tumor growth by induction of microtubule stabilization and promotion of [[ bcl-2 ]] inactivation, which induce apoptosis.

Risperidone is metabolized to its active metabolite, << 9-hydroxyrisperidone >>, mainly by the [[ cytochrome P450 ]] enzymes CYP2D6 and 3A4.

<< Risperidone >> is metabolized to its active metabolite, 9-hydroxyrisperidone, mainly by the [[ cytochrome P450 ]] enzymes CYP2D6 and 3A4.

Both << risperidone >> and 9-hydroxyrisperidone are substrates of [[ P-glycoprotein ]] (P-gp), a transport protein involved in drug absorption, distribution, and elimination.

Both << risperidone >> and 9-hydroxyrisperidone are substrates of P-glycoprotein ([[ P-gp ]]), a transport protein involved in drug absorption, distribution, and elimination.

Both risperidone and << 9-hydroxyrisperidone >> are substrates of [[ P-glycoprotein ]] (P-gp), a transport protein involved in drug absorption, distribution, and elimination.

Both risperidone and << 9-hydroxyrisperidone >> are substrates of P-glycoprotein ([[ P-gp ]]), a transport protein involved in drug absorption, distribution, and elimination.

bis(Ethyl) oligoamine analogues of polyamines, such as SL-11144 and SL-11158, as well as arylamine analogues [BW-1, a bis(phenylbenzyl) 3-7-3 analogue] blocked uptake and interconversion of spermine at micromolar levels and, in the case of << BW-1 >>, acted as substrate for [[ PAO ]].

<< SL-11158 >> inhibited [[ SSAT ]] activity with a mixed type of inhibition in which the analogue had a 70-fold higher affinity for the enzyme than the natural substrate, spermine.

Synthesis and in vitro evaluation of << N-Aryl pyrido-quinazolines >> derivatives as potent [[ EGFR ]] inhibitors.

A series of << pyrido-quinazolines >> have been synthesised, characterised and tested for their in vitro [[ EGFR ]] tyrosine kinase inhibitory activity.

A series of << pyrido-quinazolines >> have been synthesised, characterised and tested for their in vitro EGFR [[ tyrosine kinase ]] inhibitory activity.

Exposure to << Cu >> NPs decreased cell viability to 73% (p<0.01) and significantly (p<0.05) elevated levels of lactate dehydrogenase, intracellular reactive oxygen species and [[ interleukin-8 ]] that mirrored our findings from subacute in vivo inhalation studies in mice.

Exposure to << Cu >> NPs decreased cell viability to 73% (p<0.01) and significantly (p<0.05) elevated levels of [[ lactate dehydrogenase ]], intracellular reactive oxygen species and interleukin-8 that mirrored our findings from subacute in vivo inhalation studies in mice.

The Trx mimetics peptides (TXM) protected insulinoma INS 832/13 cells from oxidative stress induced by selectively inhibiting << TrxR >> with [[ auranofin ]] (AuF).

The Trx mimetics peptides (TXM) protected insulinoma INS 832/13 cells from oxidative stress induced by selectively inhibiting << TrxR >> with auranofin ([[ AuF ]]).

The TXM peptides were effective in inhibiting << AuF >>-induced [[ MAPK ]], JNK and p38(MAPK) phosphorylation, in correlation with preventing caspase-3 cleavage and thereby PARP-1 dissociation.

The TXM peptides were effective in inhibiting << AuF >>-induced MAPK, [[ JNK ]] and p38(MAPK) phosphorylation, in correlation with preventing caspase-3 cleavage and thereby PARP-1 dissociation.

The TXM peptides were effective in inhibiting << AuF >>-induced MAPK, JNK and [[ p38 ]](MAPK) phosphorylation, in correlation with preventing caspase-3 cleavage and thereby PARP-1 dissociation.

The TXM peptides were effective in inhibiting << AuF >>-induced MAPK, JNK and p38([[ MAPK ]]) phosphorylation, in correlation with preventing caspase-3 cleavage and thereby PARP-1 dissociation.

Preferential block of late sodium current in the << LQT3 DeltaKPQ mutant >> by the class I(C) antiarrhythmic [[ flecainide ]].

<< Flecainide >> block of Na(+) current (I(Na)) was investigated in wild-type (WT) or the long QT syndrome 3 (LQT3) sodium channel alpha subunit mutation with three amino acids deleted ([[ DeltaKPQ ]]) stably transfected into human embryonic kidney 293 cells using whole-cell, patch-clamp recordings.

<< Flecainide >> block of Na(+) current (I(Na)) was investigated in wild-type (WT) or the [[ long QT syndrome 3 (LQT3) sodium channel alpha ]] subunit mutation with three amino acids deleted (DeltaKPQ) stably transfected into human embryonic kidney 293 cells using whole-cell, patch-clamp recordings.

Flecainide block of Na(+) current (I(Na)) was investigated in wild-type (WT) or the << long QT syndrome 3 (LQT3) sodium channel alpha >>[[ sodium ]] channel alpha subunit mutation with three amino acids deleted (DeltaKPQ) stably transfected into human embryonic kidney 293 cells using whole-cell, patch-clamp recordings.

Compared with WT, << DeltaKPQ >> I(Na) was more sensitive to [[ flecainide ]], and flecainide preferentially inhibited late I(Na) (mean current between 20 and 23.5 ms after depolarization) compared with peak I(Na).

Compared with WT, << DeltaKPQ >> I(Na) was more sensitive to flecainide, and [[ flecainide ]] preferentially inhibited late I(Na) (mean current between 20 and 23.5 ms after depolarization) compared with peak I(Na).

We conclude that << DeltaKPQ >> interacts differently with [[ flecainide ]] than with WT, leading to increased block and slowed recovery, especially for late I(Na).

Both << 5'-AMN >> and 5'-MABN had high affinity for κ-receptors (K (i) 1.36 ± 0.98 and 0.27 ± 0.08, respectively) and were revealed as potent κ-antagonists (pA(2) 7.43 and 8.18, respectively) and [[ μ-receptor ]] antagonists (pA(2) 7.62 and 7.85, respectively) in the ileum.

Both 5'-AMN and << 5'-MABN >> had high affinity for κ-receptors (K (i) 1.36 ± 0.98 and 0.27 ± 0.08, respectively) and were revealed as potent κ-antagonists (pA(2) 7.43 and 8.18, respectively) and [[ μ-receptor ]] antagonists (pA(2) 7.62 and 7.85, respectively) in the ileum.

Polo-like kinase-2 (Plk-2) is a potential therapeutic target for Parkinson's disease and this Letter describes the SAR of a series of << dihydropteridinone >> based [[ Plk-2 ]] inhibitors.

<< Sphingosine-1-phosphate >> promotes the nuclear translocation of β-catenin and thereby induces [[ osteoprotegerin ]] gene expression in osteoblast-like cell lines.

<< S1P >> activated [[ phosphatidylinositol 3-kinase ]] (PI3K)/Akt signaling, leading to the inhibition of glycogen synthase kinase-3β and the nuclear translocation of β-catenin, followed by the increase of the transcriptional activity by β-catenin/T-cell factor complex formation in both SaOS-2 cells and MC3T3-E1 cells.

<< S1P >> activated phosphatidylinositol 3-kinase ([[ PI3K ]])/Akt signaling, leading to the inhibition of glycogen synthase kinase-3β and the nuclear translocation of β-catenin, followed by the increase of the transcriptional activity by β-catenin/T-cell factor complex formation in both SaOS-2 cells and MC3T3-E1 cells.

<< S1P >> activated phosphatidylinositol 3-kinase (PI3K)/[[ Akt ]] signaling, leading to the inhibition of glycogen synthase kinase-3β and the nuclear translocation of β-catenin, followed by the increase of the transcriptional activity by β-catenin/T-cell factor complex formation in both SaOS-2 cells and MC3T3-E1 cells.

<< S1P >> activated phosphatidylinositol 3-kinase (PI3K)/Akt signaling, leading to the inhibition of [[ glycogen synthase kinase-3β ]] and the nuclear translocation of β-catenin, followed by the increase of the transcriptional activity by β-catenin/T-cell factor complex formation in both SaOS-2 cells and MC3T3-E1 cells.

<< S1P >> increased the amount of [[ osteoprotegerin ]] at both mRNA and protein levels, and increased the activity of alkaline phosphatase, leading to the mineralization.