Analysis of Bose-Einstein correlations in e+e- -> W+W- events including final state interactions

Recently DELPHI Collaboration reported new data on Bose-Einstein correlations (BEC) measured in e+e- -> W^+W^- events. Apparently no enhancement has been observed. We have analyzed these data including final state interactions (FSI) of both Coulomb and strong (s-wave) origin and found that there is enhancement in BEC but it is overshadowed by the FSI which are extremely important for those events. We have found the following values for the size of the interaction range beta and the degree of coherence lambda: beta=0.87 +/- 0.31fm and lambda=1.19 +/- 0.48, respectively.Comment: 7pages, 4 figure

Meson-Meson Scattering in the Quark Model: Spin Dependence and Exotic Channels

We apply a quark interchange model to spin-dependent and exotic meson-meson scattering. The model includes the complete set of standard quark model forces, including OGE spin-orbit and tensor and scalar confinement spin-orbit. Scattering amplitudes derived assuming SHO and Coulomb plus linear plus hyperfine meson wavefunctions are compared. In I=2 pi pi we find approximate agreement with the S-wave phase shift from threshold to 1.5 GeV, where we predict an extremum that is supported by the data. Near threshold we find rapid energy dependence that may reconcile theoretical estimates of small scattering lengths with experimental indications of larger ones based on extrapolation of measurements at moderate kpi^2. In PsV scattering we find that the quark-quark L*S and T forces map into L*S and T meson-meson interactions, and the P-wave L*S force is large. Finally we consider scattering in J^PC-exotic channels, and note that some of the Deck effect mechanisms suggested as possible nonresonant origins of the pi_1(1400) signal are not viable in this model.Comment: 51 pages, 10 figures, uses epsf.sty epsfig.st

Analyticity, Crossing Symmetry and the Limits of Chiral Perturbation Theory

The chiral Lagrangian for Goldstone boson scattering is a power series expansion in numbers of derivatives. Each successive term is suppressed by powers of a scale, $\Lambda_\chi$, which must be less than of order $4\pi f/\sqrt{N}$ where $f$ is the Goldstone boson decay constant and $N$ is the number of flavors. The chiral expansion therefore breaks down at or below $4 \pi f/\sqrt{N}$. We argue that the breakdown of the chiral expansion is associated with the appearance of physical states other than Goldstone bosons. Because of crossing symmetry, some ``isospin'' channels will deviate from their low energy behavior well before they approach the scale at which their low energy amplitudes would violate unitarity. We argue that the estimates of ``oblique'' corrections from technicolor obtained by scaling from QCD are untrustworthy.Comment: harvmac, 18 pages (3 figures), HUTP-92/A025, BUHEP-92-18, new version fixes a TeX problem in little mod

Another look at ππ\pi\pi scattering in the scalar channel

We set up a general framework to describe $\pi\pi$ scattering below 1 GeV based on chiral low-energy expansion with possible spin-0 and 1 resonances. Partial wave amplitudes are obtained with the $N/D$ method, which satisfy unitarity, analyticity and approximate crossing symmetry. Comparison with the phase shift data in the J=0 channel favors a scalar resonance near the $\rho$ mass.Comment: 17 pages, 5 figures, REVTe

A Quark Model Calculation of gamma gamma to pi pi Including Final State Interactions

A quark model calculation of the processes gamma gamma -> pi+ pi- and gamma gamma -> pi0 pi0 is performed. At tree level, only charged pions couple to the initial state photons and neutral pions are not expected in the final state. However, a small but significant gamma gamma -> pi0 pi0 cross section is observed. We demonstrate that this may be accounted for by a rotation in isospin space induced by final state interactions. The resulting pi+ pi- cross section is in good agreement with experiment while the pi0 pi0 cross section is in qualitative agreement with the data.Comment: 22 Revtex pages, 5 postscript figure

The ππ\pi\pi Final State Interaction in K→ππK\to\pi\pi, pp→ppππpp\to pp\pi\pi and Related Processes

Final state interactions in the $S$--wave $\pi\pi$ system (I=0,2) are re-examined on the basis of the Omn\`es-Mus\-khe\-li\-shvili equation and the coupled channel formalism. The contributions to the pion scalar form factor from $\rho$ and $f_2(1270)$ exchange in the $t$--channel and from the $f_0(980)$ $s$--channel resonance are separately evaluated and the role of the nontrivial polynomial in the Omn\`es function in a coupled channel situation is elucidated. Applications are made to $K\to \pi\pi$ and $pp\to pp\pi\pi$. It is found that the contribution from the $f_0$ resonance to the form-factor is strongly reduced by a nearby zero.Comment: PACS numbers: 13.75.Lb, 13.25.Es, 13.25.+m, 15 pages in plain latex with epsf.sty, 10 figure

Myelin disorders : causes and perspectives of Charcot-Marie-Tooth neuropathy

Charcot-Marie-Tooth (CMT) disease is a common hereditary neuropathy that causes progressive distally pronounced muscle weakness and can lead to life-long disability in patients. In most cases, the disorder has been associated with a partial duplication of human chromosome 17 (CMT1A), causing 1.5-fold overexpression of the peripheral myelin protein 22 kDa (PMP22). Increased PMP22 gene dosage results in demyelination, secondary axonal loss, and neurogenic muscle atrophy. Experimental therapeutic approaches based on the role of progesterone and ascorbic acid in myelin formation recently have reached preclinical proof-of-principle trials in rodents. It was shown that progesterone receptor antagonists can reduce PMP22 overexpression and clinical severity in a CMT1A rat model. Furthermore, ascorbic acid treatment reduced premature death and demyelination in a CMT1A mouse model. Thus, basic research has opened up new vistas for the understanding and treatment of hereditary neuropathies

Progesterone antagonist therapy in a Pelizaeus-Merzbacher mouse model

Pelizaeus-Merzbacher disease (PMD) is a severe hypomyelinating disease, characterized by ataxia, intellectual disability, epilepsy, and premature death. In the majority of cases, PMD is caused by duplication of PLP1 that is expressed in myelinating oligodendrocytes. Despite detailed knowledge of PLP1, there is presently no curative therapy for PMD. We used a Plp1 transgenic PMD mouse model to test the therapeutic effect of Lonaprisan, an antagonist of the nuclear progesterone receptor, in lowering Plp1 mRNA overexpression. We applied placebo-controlled Lonaprisan therapy to PMD mice for 10 weeks and performed the grid slip analysis to assess the clinical phenotype. Additionally, mRNA expression and protein accumulation as well as histological analysis of the central nervous system were performed. Although Plp1 mRNA levels are increased 1.8-fold in PMD mice compared to wild-type controls, daily Lonaprisan treatment reduced overexpression at the RNA level to about 1.5-fold, which was sufficient to significantly improve the poor motor phenotype. Electron microscopy confirmed a 25% increase in the number of myelinated axons in the corticospinal tract when compared to untreated PMD mice. Microarray analysis revealed the upregulation of proapoptotic genes in PMD mice that could be partially rescued by Lonaprisan treatment, which also reduced microgliosis, astrogliosis, and lymphocyte infiltration