scholarly journals Strange Quark Polarization of the Nucleon: A Parameter-Independent Prediction of the Chiral Potential Model

2001 ◽  
Vol 87 (1) ◽  
Author(s):  
Xiang-Bai Chen ◽  
Xiang-Song Chen ◽  
Fan Wang
Keyword(s):  
Strange Quark ◽  
Potential Model ◽  
Chiral Potential

Magnetic moments of octet baryons in a chiral potential model

Pramana ◽  
1986 ◽  
Vol 27 (6) ◽  
pp. 783-793 ◽  
Author(s):  
N Barik ◽  
M Das
Keyword(s):  
Potential Model ◽  
Magnetic Moments ◽  
Chiral Potential ◽  
Octet Baryons

Positive and convergent self-energy in a chiral potential model

1989 ◽  
Vol 229 (4) ◽  
pp. 333-338 ◽  
Author(s):  
T. Gutsche ◽  
D. Robson
Keyword(s):  
Potential Model ◽  
Self Energy ◽  
Chiral Potential

FLAVOR-ASYMMETRIC SEA QUARK DISTRIBUTION IN A CHIRAL POTENTIAL MODEL

1998 ◽  
Vol 13 (11) ◽  
pp. 1785-1794 ◽  
Author(s):  
KAKALI ROY-MAITY ◽  
PADMANABHA DASGUPTA
Keyword(s):  
Evolution Equations ◽  
Potential Model ◽  
Quark Distribution ◽  
Structure Functions ◽  
Static Properties ◽  
Domain Of Applicability ◽  
Pion Emission ◽  
Additive Contribution ◽  
Evolution Of Structure ◽  
Chiral Potential

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.

A chiral potential model of the nucleon

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

Quark–pion coupling strength and ground state baryon spectra in a chiral potential model

2011 ◽  
Vol 89 (12) ◽  
pp. 1261-1272
Author(s):  
S.N. Jena ◽  
R.N. Mishra ◽  
P.K. Mohapatra ◽  
S. Sahoo
Keyword(s):  
Ground State ◽  
Coupling Strength ◽  
Potential Model ◽  
Baryon Spectra ◽  
Chiral Potential ◽  
State Baryon

BALB-Abcb4 mice lacking the hepatobiliary phospholipid transporter represent a potential model of hepatic osteodystrophy

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

Strange Quark Matter as Dark Matter

2019 ◽  
Vol 22 (4) ◽  
pp. 311-317
Author(s):  
Hidezumi Terazawa
Keyword(s):  
Dark Matter ◽  
Quark Matter ◽  
Strange Quark ◽  
Strange Quark Matter ◽  
Quark Stars

New forms of matter such as super-hypernuclei (strange quark matter) and superhypernuclear stars (strange quark stars) as candidates for dark matter are discussed in some detail, based on the so-called "Bodmer–Terazawa–Witten hypothesis" assuming that they are stable absolutely or quasi-stable (decaying only weakly).

RELATIVE CONTRIBUTIONS OF FIBROSIS AND CONNEXIN CHANGES TOTHE ATRIAL FIBRILLATION SUBSTRATE DURING THE DEVELOPMENT AND REVERSAL OF CONGESTIVEHEART FAILURE

2008 ◽  
Vol 31 (4) ◽  
pp. 5
Author(s):  
Brett Burstein ◽  
Kunihiro Nishida ◽  
Philippe Comtois ◽  
Louis Villenuve ◽  
Yung-Hsin Yeh ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Potential Model ◽  
Diastolic Pressure ◽  
Recovery Period ◽  
Left Ventricular ◽  
Muscle Bundle ◽  
Protein Ratio ◽  
Conduction Disturbances ◽  
Conduction Abnormalities ◽  
Mrna And Protein Expression

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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