The $$(q\bar q) - pion$$ and its decay constant in a chiral potential modeland its decay constant in a chiral potential model

Pramana ◽  
1987 ◽  
Vol 29 (6) ◽  
pp. 543-557 ◽  
Author(s):  
N Barik ◽  
B K Dash ◽  
P C Dash
2009 ◽  
Vol 87 (11) ◽  
pp. 1171-1180
Author(s):  
S. N. Jena ◽  
M. K. Muni ◽  
H. R. Pattnaik

The mass and decay constant of the [Formula: see text]-pion together with the masses of ρ and ω mesons are calculated in a chiral symmetric potential model of independent quarks, taking into account the corrections due to the possible residual interactions, such as quark–pion coupling arising out of the requirement of chiral symmetry and quark gluon coupling arising out of one-gluon-exchange, and that due to the spurious center-of-mass motion of the meson core. The effective potential representing phenomenologically the nonperturbative gluon interactions, including gluon self coupling, is chosen with equally mixed scalar and vector parts in a logarithmic form. The result obtained for the physical mass of [Formula: see text]-pion is consistent with that of the PCAC-pion, and the pion-decay constant reasonably agrees with experiment.


Pramana ◽  
1986 ◽  
Vol 27 (6) ◽  
pp. 783-793 ◽  
Author(s):  
N Barik ◽  
M Das

1989 ◽  
Vol 229 (4) ◽  
pp. 333-338 ◽  
Author(s):  
T. Gutsche ◽  
D. Robson

1998 ◽  
Vol 13 (11) ◽  
pp. 1785-1794 ◽  
Author(s):  
KAKALI ROY-MAITY ◽  
PADMANABHA DASGUPTA

Flavor asymmetry of the sea quark distribution which expresses itself in the observed value of the Gottfried sum leads one to consider pion emission as directly contributing to the scale dependence of structure functions. As an example, we study the evolution of structure functions in a chiral potential model which incorporates the pion as the chiral-symmetry-restoring field and which was originally invented to explain the static properties of baryons. Evolution equations for the quark and pion densities are derived in the lowest order at subasymptotic Q2. The kernels of evolution for the effective quark densities turn out to be flavor-dependent and are endowed with properties quite distinct from those possessed by leading log QCD splitting functions. In particular, the commonly used probabilistic treatment of the evolution, which is legitimate in the kinematic region of the perturbative QCD evolution, is seen not to be valid in the domain of applicability of the chiral potential model. The model is shown to lead to nontrivial evolution of the nonsinglet moments in a manner consistent with the observed departure from the Gottfried sum rule in a low Q2 region. For higher Q2, the evolution of the Gottfried sum receives also an additive contribution not envisaged in the earlier works on the phenomenon.


1986 ◽  
Vol 168 (4) ◽  
pp. 309-312 ◽  
Author(s):  
J.M. Greben ◽  
M. Araki

2011 ◽  
Vol 89 (12) ◽  
pp. 1261-1272
Author(s):  
S.N. Jena ◽  
R.N. Mishra ◽  
P.K. Mohapatra ◽  
S. Sahoo

Pramana ◽  
1998 ◽  
Vol 51 (6) ◽  
pp. 711-725 ◽  
Author(s):  
S. N. Jena ◽  
M. R. Behera ◽  
S. Panda

2009 ◽  
Vol 47 (09) ◽  
Author(s):  
K Hochrath ◽  
B Rathkolb ◽  
K Butuzova ◽  
W Hans ◽  
H Fuchs ◽  
...  

2008 ◽  
Vol 31 (4) ◽  
pp. 5
Author(s):  
Brett Burstein ◽  
Kunihiro Nishida ◽  
Philippe Comtois ◽  
Louis Villenuve ◽  
Yung-Hsin Yeh ◽  
...  

Background: Connexin alterations occur in various atrial fibrillation (AF) paradigms, but their functional significance remains unclear. No data are available regarding the effects of CHF on atrial connexin expression and phosphorylation. We therefore analyzed connexin changes and their contribution to the AF substrate during the development and reversal ofCHF. Methods and Results: Dogs were allocated to three groups: CHF induced by 2-week ventricular tachypacing (CHF, n=15); CHF dogs allowed to recover for 4 weeks after 2-week tachypacing (REC, n=15) and non-paced shams (CTL, n=11). Left ventricular end-diastolic pressure increased with CHF (14.5±1.0*** vs.3.7±0.7, ***P < 0.001 vs. CTL) and normalized upon CHF recovery (5.1±1.0^†††, ^††† P < 0.001 vs. CHF). Real-time PCR and Western-blot analyses revealed connexin43 (Cx43) and connexin40 (Cx40) mRNA and protein expression to be unchanged by CHF and REC. However, CHF caused Cx43 dephosphorylation(by ~73%***) and increased Cx40/Cx43 protein ratio (by ~35%***), with both alterations completely reversing in REC. Immunofluorescent confocal microscopy confirmed connexin protein trends, with a reduction in phosphorylated Cx43 (by ~68%*** in CHF) that returned to control in REC. CHF caused conduction abnormalities (phasedelay-range and heterogeneity index, both P < 0.01) and burst pacing-induced AF prolongation (CTL 22±7s, CHF 1100±171s***, REC 884±220s***) which persisted in the recovery period, along with residual fibrosis (CTL 3.6±0.7%, CHF 14.7±1.5%***, REC13.3±2.3%***). Fibrosis physically interrupted muscle bundle continuity and anionically-based action potential model of canine atrium showed that fibrosiswas able to account for the observed conduction abnormalities. Conclusions: CHF causes connexin-dephosphorylation and Cx40/Cx43ratio increases. With CHF reversal, atrial connexin alterations recover completely, but tissue fibrosis, conduction abnormalities and a substrate forAF remain with fibrosis accounting for conduction abnormalities. Thus, althougha trial connexin changes occur with CHF, they are not essential for conduction disturbances and AF promotion, which appear rather to be related primarily tofibrotic interruption of muscle-bundle continuity.


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