Long-distance dispersal of pigeons and doves generated new ecological opportunities for host-switching and adaptive radiation by their parasites.

Adaptive radiation is an important mechanism of organismal diversification and can be triggered by new ecological opportunities. Although poorly studied in this regard, parasites are an ideal group in which to study adaptive radiations because of their close associations with host species. Both experimental and comparative studies suggest that the ectoparasitic wing lice of pigeons and doves have adaptively radiated, leading to differences in body size and overall coloration. Here, we show that long-distance dispersal by dove hosts was central to parasite diversification because it provided new ecological opportunities for parasites to speciate after host-switching. We further show that among extant parasite lineages host-switching decreased over time, with cospeciation becoming the more dominant mode of parasite speciation. Taken together, our results suggest that host dispersal, followed by host-switching, provided novel ecological opportunities that facilitated adaptive radiation by parasites

Ballistic electron motion in a random magnetic field

Using a new scheme of the derivation of the non-linear $\sigma$-model we consider the electron motion in a random magnetic field (RMF) in two dimensions. The derivation is based on writing quasiclassical equations and representing their solutions in terms of a functional integral over supermatrices $Q$ with the constraint $Q^2=1$. Contrary to the standard scheme, neither singling out slow modes nor saddle-point approximation are used. The $\sigma$-model obtained is applicable at the length scale down to the electron wavelength. We show that this model differs from the model with a random potential (RP).However, after averaging over fluctuations in the Lyapunov region the standard $\sigma$-model is obtained leading to the conventional localization behavior.Comment: 10 pages, no figures, to be submitted in PRB v2: Section IV is remove

Magnetoresistance and dephasing in a two-dimensional electron gas at intermediate conductances

We study, both theoretically and experimentally, the negative magnetoresistance (MR) of a two-dimensional (2D) electron gas in a weak transverse magnetic field $B$. The analysis is carried out in a wide range of zero-$B$ conductances $g$ (measured in units of $e^2/h$), including the range of intermediate conductances, $g\sim 1$. Interpretation of the experimental results obtained for a 2D electron gas in GaAs/In$_x$Ga$_{1-x}$As/GaAs single quantum well structures is based on the theory which takes into account terms of higher orders in $1/g$, stemming from both the interference contribution and the mutual effect of weak localization (WL) and Coulomb interaction. We demonstrate that at intermediate conductances the negative MR is described by the standard WL "digamma-functions" expression, but with a reduced prefactor $\alpha$. We also show that at not very high $g$ the second-loop corrections dominate over the contribution of the interaction in the Cooper channel, and therefore appear to be the main source of the lowering of the prefactor, $\alpha\simeq 1-2/\pi g$. We further analyze the regime of a "weak insulator", when the zero-$B$ conductance is low $g(B=0)<1$ due to the localization at low $T$, whereas the Drude conductance is high, $g_0>>1.$ In this regime, while the MR still can be fitted by the digamma-functions formula, the experimentally obtained value of the dephasing rate has nothing to do with the true one. The corresponding fitting parameter in the low-$T$ limit is determined by the localization length and may therefore saturate at $T\to 0$, even though the true dephasing rate vanishes.Comment: 36 pages, 16 figure

Rapid entry and downregulation of T Cells in the central nervous system During the reinduction of experimental autoimmune encephalomyelitis

We investigated the mechanisms whereby a previous attack of experimental autoimmune encephalomyelitis (EAE) modifies a subsequent attack in the Lewis rat. Active immunization with myelin basic protein (MBP) and complete Freund's adjuvant 28 days after the passive transfer of MBP-sensitized spleen cells induced a second episode of EAE, which occurred earlier than in naive control animals, but was less severe overall. The pattern of neurological signs was also different in rechallenged rats, which had less severe tail and hindlimb weakness but more severe forelimb weakness. In rechallenged rats, inflammation was more severe in the cervical spinal cord, cerebellum, brainstem and cerebrum, but less severe in the lumbar spinal cord, than in controls. The early onset of EAE in rechallenged rats was explained by a memory T cell response to MBP72-89 in the draining lymph node and spleen, and by the enhanced entry of T cells into the central nervous system (CNS). However, the number of alpha beta T cells in the spinal cord of rechallenged rats declined faster than in controls, especially in the lumbosacral cord, where the number of V beta 8.2+ T cells and the frequency of T cells reactive to MBP72-89 rapidly decreased, indicating rapid downregulation of the immune response in the previously inflamed spinal cord. Apoptosis of inflammatory cells in the CNS was increased in the rechallenged rats and is likely to contribute to this downregulation. Furthermore, during the disease course the generation of encephalitogenic T cells in the peripheral lymphoid organs was limited compared with controls. Thus, a previous attack of EAE modifies a subsequent attack through the interaction of the following processes: a memory T cell response to MBP; facilitated T cell entry into the CNS; downregulation of the immune response in the CNS, including increased apoptosis of inflammatory cells; and a limited generation of encephalitogenic T cells in the peripheral lymphoid organs

Apoptosis in the Nervous System in Experimental Allergic Encephalomyelitis

We report here for the first time the occurrence of apoptosis of cells in the spinal cord in experimental allergic encephalomyelitis (EAE), an autoimmune, T-cell-mediated demyelinating disease. Four different forms of EAE were studied in the Lewis rat: (i) acute EAE induced by inoculation with whole spinal cord and adjuvants; (ii) acute EAE induced by inoculation with myelin basic protein (MBP) and adjuvants; (iii) acute EAE induced by the passive transfer of MBP-sensitized spleen cells; (iv) chronic relapsing EAE induced by inoculation with whole spinal cord and adjuvants followed by treatment with low-dose cyclosporin A. Cells undergoing apoptosis were recognized at light and electron microscopy by the presence of either crescentic masses of condensed chromatin lying against the nuclear envelope or rounded masses of uniformly dense chromatin. They were found in both the white and grey matter of the spinal cord in all 4 forms of this disease. Although it was not possible to identify definitively the types of cells undergoing apoptosis, the size and location of some of the affected cells suggested that they were oligodendrocytes. As there is now a large body of evidence that T-cell-induced target cell death takes the form of apoptosis, it is attractive to hypothesize that oligodendrocyte apoptosis is occurring in EAE as a result of oligodendrocyte-directed T-cell cytotoxicity. However, other apoptotic cells were located within the myelin sheath, meninges and perivascular spaces and were clearly not oligodendrocytes but were most likely blood-derived mononuclear cells. The sparsity of their cytoplasm and the absence of phagocytosed material suggested that they were mainly lymphocytes rather than macrophages. Apoptosis has been shown to be involved in deleting autoreactive T-cells during the normal development of tolerance. Thus apoptotic deletion of myelin/oligodendrocyte-specific lymphocytes in the central nervous system in EAE might explain both the subsidence of inflammation and the acquisition of tolerance in this autoimmune disease

Number--conserving model for boson pairing

An independent pair ansatz is developed for the many body wavefunction of dilute Bose systems. The pair correlation is optimized by minimizing the expectation value of the full hamiltonian (rather than the truncated Bogoliubov one) providing a rigorous energy upper bound. In contrast with the Jastrow model, hypernetted chain theory provides closed-form exactly solvable equations for the optimized pair correlation. The model involves both condensate and coherent pairing with number conservation and kinetic energy sum rules satisfied exactly and the compressibility sum rule obeyed at low density. We compute, for bulk boson matter at a given density and zero temperature, (i) the two--body distribution function, (ii) the energy per particle, (iii) the sound velocity, (iv) the chemical potential, (v) the momentum distribution and its condensate fraction and (vi) the pairing function, which quantifies the ODLRO resulting from the structural properties of the two--particle density matrix. The connections with the low--density expansion and Bogoliubov theory are analyzed at different density values, including the density and scattering length regime of interest of trapped-atoms Bose--Einstein condensates. Comparison with the available Diffusion Monte Carlo results is also made.Comment: 21 pages, 12 figure

Towards Noncommutative Fuzzy QED

We study in one-loop perturbation theory noncommutative fuzzy quenched QED_4. We write down the effective action on fuzzy S**2 x S**2 and show the existence of a gauge-invariant UV-IR mixing in the model in the large N planar limit. We also give a derivation of the beta function and comment on the limit of large mass of the normal scalar fields. We also discuss topology change in this 4 fuzzy dimensions arising from the interaction of fields (matrices) with spacetime through its noncommutativity.Comment: 33 page

Demyelination and Early Remyelination in Experimental Allergic Encephalomyelitis Passively Transferred With Myelin Basic Protein-Sensitized Lymphocytes in the Lewis Rat

Histological studies were performed on Lewis rats with experimental allergic encephalomyelitis (EAE) passively transferred by myelin basic protein (MBP)-sensitized syngeneic spleen cells in order to determine the relationship between demyelination and neurological signs. Neither inflammation nor demyelination was present on the day prior to the onset of neurological signs but both were present in the spinal roots and spinal cord on the day of onset of tail weakness (4 days after passive transfer). Demyelination and the neurological signs both increased over the next 48 h. There was evidence that the caudal roots were more severely affected than the rostral roots. The peripheral nerves were spared. Demyelination in the spinal cord was concentrated in the dorsal root entry and ventral root exit zones. The initial stages of repair of demyelinated spinal root fibres by Schwann cells were observed on the earliest day that clinical recovery commenced (day 7). At this time some demyelinated fibres were closely associated with debris-free Schwann cells, and occasional fibres were completely invested by 1-2 layers of Schwann cell cytoplasm. Remyelination (compact myelin lamellae formation) by Schwann cells was first observed in the spinal roots on day 9. By the time of complete clinical recovery (day 11) the majority of affected spinal root fibres had thin new myelin sheaths. Repair of central nervous system myelin by oligodendrocytes was slower than peripheral nervous system myelin repair. Investment of demyelinated spinal cord axons by oligodendrocytes was observed on day 9, and remyelination by these cells was seen on day 10. We conclude that the neurological signs of passively induced MBP-EAE can be accounted for by demyelination of the lumbar, sacral and coccygeal spinal roots and spinal cord root entry and exit zones, and that the subsequent clinical recovery can be explained by investment and remyelination of demyelinated peripheral and central nervous system fibres by Schwann cells and oligodendrocytes respectively

Charm System Tests of CPT and Lorentz Invariance with FOCUS

We have performed a search for CPT violation in neutral charm meson oscillations. While flavor mixing in the charm sector is predicted to be small by the Standard Model, it is still possible to investigate CPT violation through a study of the proper time dependence of a CPT asymmetry in right-sign decay rates for $D^0\to K^-\pi^+$ and \d0b\to K^+\pi^-. This asymmetry is related to the CPT violating complex parameter $\xi$ and the mixing parameters $x$ and $y$: $A_{CPT}\propto{\rm Re} \xi y-{\rm Im} \xi x$ . Our 95% confidence level limit is $-0.0068<{\rm Re} \xi y-{\rm Im} \xi x<0.0234$. Within the framework of the Standard Model Extension incorporating general CPT violation, we also find 95% confidence level limits for the expressions involving coefficients of Lorentz violation of $(-2.8<N(x,y,\delta)(\Delta a_0 + 0.6 \Delta a_Z)<4.8)\times 10^{-16}$ GeV, $(-7.0<N(x,y,\delta)\Delta a_X<3.8)\times 10^{-16}$ GeV, and $(-7.0<N(x,y,\delta)\Delta a_Y<3.8)\times 10^{-16}$ GeV, where $N(x,y,\delta)$ is the factor which incorporates mixing parameters $x$, $y$ and the doubly Cabibbo suppressed to Cabibbo favored relative strong phase $\delta$.Comment: 12 pages 5 figure

K2 and Spitzer phase curves of the rocky ultra-short-period planet K2-141 b hint at a tenuous rock vapor atmosphere

Stars and planetary system