We present results for the photoionization of ground and excited S states of two-electron systems byx-ray photons. The method uses the asymptotic formulation of Dalgarno and Stewart [Proc. Phys. Soc. London 76, 49 (1960)] with highly correlated Frankowski-Pekeris -type wave functions for N 'S and N 'S initial states. The calculations show a smaller ratio of double-to-single photoionization R for triplet states due to the spatial antisymmetry of the wave function near the nucleus. We find an asymmetric population of photoion satellite states and provide expressions for the asymptotic single and total photoionization, and R as a function of nuclear charge. We also make predictions for the differential double photoionization cross sections in the extreme energy sharing case when one electron is ejected with zero energy.PACS number(s): 32.80.Fb, 32.30.Rj, 32.70.Cs I. INTRGDUCTIQNConsiderable attention has been given recently in experimental [1 -3] and theoretical [4 -8] studies to the double ionization of the ground state of helium by the absorption of a high-frequency photon. The double photoionization (DPI) of the other members of the helium sequence and of the metastable 2 S states of helium have also been investigated [5,9,10]. It has been established that the ratio of the double-to-single photoionization cross section tends to a constant at high frequencies. The asymptotic ratio can be calculated accurately in the acceleration form of the electric-dipole operator, provided that electron-electron correlation is adequately represented in the initial state wave function [11].In this paper, we employ fully correlated initial state wave functions for the ground and excited 'S and S states of helium to predict the asymptotic ratios for single and double photoionization.We use an extrapolation of the simultaneous excitation and ionization cross sections in the double-ionization limit to obtain the differential cross section for double photoionization in which one electron is ejected with zero energy. To explore further the role of electron-electron correlation, we investigate Electronic address: rcf@cfaitamp. harvard. edu tElectronic address: hrs@cfaitamp. harvard. edu the dependence of the ratios and cross sections on the nuclear charge Z. II. THKGRY A. Asymptotic formulationThe fundamental physical photoexcitation-ionization process quantity in the A'co+He(X ' S)~He+(ns)+e is the continuum dipole oscillator strength n ""=2co( (P"(r"r,)~X d~e(r, , r, ) ) (', where~and e are the respective energies of the photon and ionized electron in atomic units and R is the direction of linearly polarized light. %(r&, r2) represents a fully correlated initial state wave function, which is denoted by %(r"rz, r, )2for S states, and g"(r"r2) is the final state product wave function for a continuum electron and a hydrogenic s-state electron with principle quantum number n. The coordinates rj and r2 are the electronic distances from the nucleus, and r, 2 is the interelectronic distance. By Fourier transforming the acceleration form of ...
Nociceptive Transient Receptor Potential channels such as TRPV1 are targets for treating pain. Both antagonism and agonism of TRP channels can promote analgesia, through inactivation and chronic desensitization. Since plant-derived mixtures of cannabinoids and the Cannabis component myrcene have been suggested as pain therapeutics, we screened terpenes found in Cannabis for activity at TRPV1. We used inducible expression of TRPV1 to examine TRPV1-dependency of terpene-induced calcium flux responses. Terpenes contribute differentially to calcium fluxes via TRPV1 induced by Cannabis-mimetic cannabinoid/terpenoid mixtures. Myrcene dominates the TRPV1-mediated calcium responses seen with terpenoid mixtures. Myrcene-induced calcium influx is inhibited by the TRPV1 inhibitor capsazepine and Myrcene elicits TRPV1 currents in the wholecell patch-clamp configuration. TRPV1 currents are highly sensitive to internal calcium. When Myrcene currents are evoked, they are distinct from capsaicin responses on the basis of I max and their lack of shift to a pore-dilated state. Myrcene pre-application and residency at TRPV1 appears to negatively impact subsequent responses to TRPV1 ligands such as Cannabidiol, indicating allosteric modulation and possible competition by Myrcene. Molecular docking studies suggest a non-covalent interaction site for Myrcene in TRPV1 and identifies key residues that form partially overlapping Myrcene and Cannabidiol binding sites. We identify several non-Cannabis plantderived sources of Myrcene and other compounds targeting nociceptive TRPs using a data mining approach focused on analgesics suggested by non-Western Traditional Medical Systems. These data establish TRPV1 as a target of Myrcene and suggest the therapeutic potential of analgesic formulations containing Myrcene.
Purpose To determine if cycle training of sedentary subjects would increase the expression of the principle muscle glucose transporters, six volunteers completed six weeks of progressively increasing intensity stationary cycle cycling. Methods In vastus lateralis muscle biopsies, changes in expression of GLUT1, GLUT4, GLUT5, and GLUT12 were compared using quantitative immunoblots with specific protein standards. Regulatory pathway components were evaluated by immunoblots of muscle homogenates and immunohistochemistry of microscopic sections. Results GLUT1 was unchanged, GLUT4 increased 66%, GLUT12 increased 104%, and GLUT5 decreased 72%. A mitochondrial marker (cytochrome c) and regulators of mitochondrial biogenesis (PGC-1α and phospho-AMPK) were unchanged, but the muscle hypertrophy pathway component, phospho-mTOR increased 83% after the exercise program. In baseline biopsies, GLUT4 by immunohistochemical techniques was 37% greater in Type I (slow twitch, red) muscle fibers, but the exercise training increased GLUT4 expression in Type II (fast twitch, white) fibers by 50%, achieving parity with the Type I fibers. Baseline phospho-mTOR expression was 50% higher in Type II fibers and increased more in Type II fibers (62%) with training, but also increased in Type I fibers (34%). Conclusion Progressive intensity stationary cycle training of previously sedentary subjects increased muscle insulin-responsive glucose transporters (GLUT4 and GLUT12) and decreased the fructose transporter (GLUT5). The increase in GLUT4 occurred primarily in Type II muscle fibers and this coincided with activation of the mTOR muscle hypertrophy pathway. There was little impact on Type I fiber GLUT4 expression and no evidence of change in mitochondrial biogenesis.
Heavy kava beverage consumption was associated with significantly elevated GGT levels.
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