A. N. Vasil’ev

Proof of the absence of multiplicative renormalizability of the Gross-Neveu model in the dimensional regularizationd=2+2ɛ

AbstractWe prove that the simplest four-fermion Gross-Neveu model with the dimensional regularization d=2+2ɛ is not multiplicatively renormalizable. This is due to the counter-term, generated by the three-loop vertex diagrams, that is proportional to the evanescent operator

Self-similar solution to the problem of vapor diffusion toward the droplet nucleated and growing in a vapor-gas medium

V_3 = (\bar \psi \gamma _{ikl}^3 \psi )^2 /2

Chronic Actions of Nicotine on the Electrogenic Activity of Na + ,K + -ATPase and the Contractile Characteristics of Rat Diaphragm

. Here

Supersaturated Vapor Recondensation : Analytical Theories and Numerical Calculation

\gamma _{i_{1 \cdots i_n } }^{(n)}

Dispersion of the speed of sound and absorption in the vicinity of the liquid-gas critical point: Renormalization-group calculation in the two-loop approximation

is the totally antisymmetric product of n γ-matrices, which is not zero in a noninteger dimension as well. Therefore, calculations of the (2+ɛ)-expansion of the critical indices η and ν in the framework of the simple Gross-Neveu model are correct only up to ε4 for η and to ɛ3 for ν. In higher orders, one must take into consideration the generation of other (not only V3) evanescent operators.

Erratum: Anomalous exponents to orderɛ3in the rapid-change model of passive scalar advection [Phys. Rev. E63, 025303 (2001)]

Methyl-β-cyclodextrin (0.1 mM) reduced resting potential of muscle fibers and abolished local endplate membrane hyperpolarization in rat diaphragm. This effect was associated with selective reduction of electrogenic activity of α2-isoform of Na,K-ATPase without changes in the level of intracellular acetylcholine. Experiments with cholesterol marker filipin showed that methyl-β-cyclodextrin in this dose induced cholesterol translocation from lipid rafts to liquid phase of the membrane without its release into extracellular space. This modification of lipid rafts by methyl-β-cyclodextrin presumably impaired the mechanism maintaining electrogenesis in endplates mediated by modulation of Na,K-ATPase by non-quantum acetylcholine. Cholesterol can serve as a molecular component of this mechanism.