24 research outputs found
Probing exotic phenomena at the interface of nuclear and particle physics with the electric dipole moments of diamagnetic atoms: A unique window to hadronic and semi-leptonic CP violation
The current status of electric dipole moments of diamagnetic atoms which
involves the synergy between atomic experiments and three different theoretical
areas -- particle, nuclear and atomic is reviewed. Various models of particle
physics that predict CP violation, which is necessary for the existence of such
electric dipole moments, are presented. These include the standard model of
particle physics and various extensions of it. Effective hadron level combined
charge conjugation (C) and parity (P) symmetry violating interactions are
derived taking into consideration different ways in which a nucleon interacts
with other nucleons as well as with electrons. Nuclear structure calculations
of the CP-odd nuclear Schiff moment are discussed using the shell model and
other theoretical approaches. Results of the calculations of atomic electric
dipole moments due to the interaction of the nuclear Schiff moment with the
electrons and the P and time-reversal (T) symmetry violating
tensor-pseudotensor electron-nucleus are elucidated using different
relativistic many-body theories. The principles of the measurement of the
electric dipole moments of diamagnetic atoms are outlined. Upper limits for the
nuclear Schiff moment and tensor-pseudotensor coupling constant are obtained
combining the results of atomic experiments and relativistic many-body
theories. The coefficients for the different sources of CP violation have been
estimated at the elementary particle level for all the diamagnetic atoms of
current experimental interest and their implications for physics beyond the
standard model is discussed. Possible improvements of the current results of
the measurements as well as quantum chromodynamics, nuclear and atomic
calculations are suggested.Comment: 46 pages, 19 tables and 16 figures. A review article accepted for
EPJ
1-Benzyl-N-[3-[spiroisobenzofuran-1(3H), 4′-piperidin-1-yl]propyl]pyrrolidine-2-carboxamide (Compound 24) antagonizes NOP receptor-mediated potassium channel activation in rat periaqueductal gray slices
Nociceptin/orphanin FQ (N/OFQ) peptide (NOP) receptor, the fourth member of opioid receptor family, shares
60–70% homology with traditional opioid receptors but displays little affinity for opioids. This receptor was
implicated in many neurological functions and its functional heterogeneity has been proposed. Therefore, it is
imperative to develop and characterize new ligands for NOP receptors. 1-Benzyl-N-[3-[spiroisobenzofuran-1
(3H),4′-piperidin-1-yl]propyl]pyrrolidine-2-carboxamide (Compound 24) is a new non-peptide ligand of
NOP receptor having antagonistic actions in cloned and peripheral NOP receptors. In this study, we
quantitatively characterized its effect on the native NOP receptors in the midbrain slices containing
ventrolateral periaqueductal gray (vlPAG), a region with dense NOP receptors and involved in pain regulation.
In vlPAG neurons, N/OFQ induced G-protein-coupled inwardly rectifying potassium (GIRK) current through
NOP receptors. Compound 24, at 0.3–10 μM, attenuated N/OFQ-induced GIRK current concentrationdependently.
The antagonistic potency of Compound 24 in vlPAG neurons (IC50: 2.6±0.6 μM) was, however,
lower than that obtained in mouse vas deferens preparations or expressed human NOP receptors. The
action kinetic of Compound 24 was slower than [Nphe1, Arg14, Lys15]N/OFQ-NH2 (UFP-101), a peptide
antagonist, in the same preparation. Compound 24 had no intrinsic agonistic activity at NOP receptors at the
concentration up to 10 μM. However, at concentrations higher than 3 μM, it also attenuated the GIRK current
induced by [D-Ala2, N-Me-Phe4, Gly5-ol]-enkephalin, a mu-opioid receptor agonist. It is concluded that
Compound 24 acts as a pure antagonist at the native NOP receptors in the vlPAG with moderate potency and
selectivity
HGF increases cisplatin resistance via down-regulation of AlF in lung cancer cells
Our previous study had shown that advanced stages of lung adenocarcinomas (ADC) was frequently associated with overexpression of hepatocyte growth factor (HGF), which has multipotent and antiapoptotic activities. In this study, we examined the effect of HGF on gene expression of apoptosis-inducing factor (AIF) and cisplatin sensitivity in lung ADC cells. Expression of AIF was determined by immunocytochemistry and confocal immunofluorescence microscopy. Our data show that addition of HGF suppressed AIF expression and increased cisplatin resistance. The effect could be through HGF receptor and its downstream effector, focal adhesion kinase (FAK). Interestingly, knockout of FAK gene increased AIF expression and drug sensitivity. Re-introduction of FAK gene, on the other hand, restored drug resistance. These results suggested that HGF might induce cisplatin resistance via c-Met to activate FAK and down-regulate AIF expression