360 research outputs found

    Forchhammeria and Stixis (Brassicales): Stem and Wood Anatomical Diversity, Ecological and Phylogenetic Significance

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    Qualitative and quantitative data are given for wood anatomy of six of the 11 recognized species of Forchhammeria (Mexico, Central America, West Indies), a genus formerly placed in Capparaceae. Though still in Brassicales, the genus has been excluded, along with several other genera, from the major recognized families of that order on the basis of molecular data. Liquid-preserved material of several species permitted detailed histological accounts of the successive cambia and their development in the stems of Forchhammeria. Successive cambia have a curious distribution in Brassicales that may represent homoplasies. Most wood features of the genus do not appear highly xeromorphic, but presence of tracheids as a wood background tissue and abundance of starch and perhaps water storage in ray parenchyma and conjunctive tissue can be cited as mechanisms likely to resist embolism formation. Forchhammeria retains green leaves throughout the dry season. Forchhammeria tamaulipana, known only from Tamaulipas State, Mexico, the single species of a new subgenus, Pauciflora, is newly described. Its embryos have nearly equal cotyledons and germinate epigeously, whereas all remaining species of the genus are pseudomonocotylous and hypogeous. These and other distinctive features of F. tamaulipana may prove significant in providing links to other brassicalean genera. The family name Stixaceae Doweld is now appropriate for Forchhammeria, Neothorelia, Stixis, and Tirani

    Quantum kinetics and thermalization in an exactly solvable model

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    We study the dynamics of relaxation and thermalization in an exactly solvable model with the goal of understanding the effects of off-shell processes. The focus is to compare the exact evolution of the distribution function with different approximations to the relaxational dynamics: Boltzmann, non-Markovian and Markovian quantum kinetics. The time evolution of the distribution function is evaluated exactly using two methods: time evolution of an initially prepared density matrix and by solving the Heisenberg equations of motion. There are two different cases that are studied in detail: i) no stable particle states below threshold of the bath and a quasiparticle resonance above it and ii) a stable discrete exact `particle' state below threshold. For the case of quasiparticles in the continuum (resonances) the exact quasiparticle distribution asymptotically tends to a statistical equilibrium distribution that differs from a simple Bose-Einstein form as a result of off-shell processes. In the case ii), the distribution of particles does not thermalize with the bath. We study the kinetics of thermalization and relaxation by deriving a non-Markovian quantum kinetic equation which resums the perturbative series and includes off-shell effects. A Markovian approximation that includes off-shell contributions and the usual Boltzmann equation are obtained from the quantum kinetic equation in the limit of wide separation of time scales upon different coarse-graining assumptions. The relaxational dynamics predicted by the non-Markovian, Markovian and Boltzmann approximations are compared to the exact result of the model. The Boltzmann approach is seen to fail in the case of wide resonances and when threshold and renormalization effects are important.Comment: 49 pages, LaTex, 17 figures (16 eps figures

    Genetic Diversity and Population Structure of the Secondary Symbiont of Tsetse Flies, Sodalis glossinidius, in Sleeping Sickness Foci in Cameroon

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    Human African trypanosomiasis remains a threat to the poorest people in Africa. The trypanosomes causing the disease are transmitted by tsetse flies. The drugs currently used are unsatisfactory: some are toxic and all are difficult to administer. Furthermore, drug resistance is increasing. Therefore, investigations for novel disease control strategies are urgently needed. Previous analyses showed the association between the presence of Glossina symbiont, Sodalis glossinidius, and the fly infection by trypanosomes in a south-western region in Cameroon: flies harbouring symbionts had a threefold higher probability of being infected by trypanosomes than flies devoid of symbionts. But the study also showed substantial differences in S. glossinidius and trypanosome infection rates between Glossina populations from two Cameroonian foci of sleeping sickness. We hypothesized that the geographical isolation of the two foci may have induced the independent evolution of each one, leading to the diversification of symbiont genotypes. Microsatellite markers were used and showed that genetic diversity structuring of S. glossinidius varies at different geographical scales with a low but significant differentiation between the Campo and Bipindi HAT foci. This encourages further work on interactions between S. glossinidius subpopulations and Glossina species that could favor tsetse fly infections by a given trypanosome species

    Functional Characterization of Human Cancer-Derived TRKB Mutations

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    Cancer originates from cells that have acquired mutations in genes critical for controlling cell proliferation, survival and differentiation. Often, tumors continue to depend on these so-called driver mutations, providing the rationale for targeted anticancer therapies. To date, large-scale sequencing analyses have revealed hundreds of mutations in human tumors. However, without their functional validation it remains unclear which mutations correspond to driver, or rather bystander, mutations and, therefore, whether the mutated gene represents a target for therapeutic intervention. In human colorectal tumors, the neurotrophic receptor TRKB has been found mutated on two different sites in its kinase domain (TRKBT695I and TRKBD751N). Another site, in the extracellular part of TRKB, is mutated in a human lung adenocarcinoma cell line (TRKBL138F). Lastly, our own analysis has identified one additional TRKB point mutation proximal to the kinase domain (TRKBP507L) in a human melanoma cell line. The functional consequences of all these point mutations, however, have so far remained elusive. Previously, we have shown that TRKB is a potent suppressor of anoikis and that TRKB-expressing cells form highly invasive and metastatic tumors in nude mice. To assess the functional consequences of these four TRKB mutations, we determined their potential to suppress anoikis and to form tumors in nude mice. Unexpectedly, both colon cancer-derived mutants, TRKBT695I and TRKBD751N, displayed reduced activity compared to that of wild-type TRKB. Consistently, upon stimulation with the TRKB ligand BDNF, these mutants were impaired in activating TRKB and its downstream effectors AKT and ERK. The two mutants derived from human tumor cell lines (TRKBL138F and TRKBP507L) were functionally indistinguishable from wild-type TRKB in both in-vitro and in-vivo assays. In conclusion, we fail to detect any gain-of-function of four cancer-derived TRKB point mutations

    SKA2 regulated hyperactive secretory autophagy drives neuroinflammation-induced neurodegeneration

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    High levels of proinflammatory cytokines induce neurotoxicity and catalyze inflammation-driven neurodegeneration, but the specific release mechanisms from microglia remain elusive. Here we show that secretory autophagy (SA), a non-lytic modality of autophagy for secretion of vesicular cargo, regulates neuroinflammation-mediated neurodegeneration via SKA2 and FKBP5 signaling. SKA2 inhibits SA-dependent IL-1β release by counteracting FKBP5 function. Hippocampal Ska2 knockdown in male mice hyperactivates SA resulting in neuroinflammation, subsequent neurodegeneration and complete hippocampal atrophy within six weeks. The hyperactivation of SA increases IL-1β release, contributing to an inflammatory feed-forward vicious cycle including NLRP3-inflammasome activation and Gasdermin D-mediated neurotoxicity, which ultimately drives neurodegeneration. Results from protein expression and co-immunoprecipitation analyses of male and female postmortem human brains demonstrate that SA is hyperactivated in Alzheimer's disease. Overall, our findings suggest that SKA2-regulated, hyperactive SA facilitates neuroinflammation and is linked to Alzheimer's disease, providing mechanistic insight into the biology of neuroinflammation

    Anomalous Kinetics of Hard Charged Particles: Dynamical Renormalization Group Resummation

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    We study the kinetics of the distribution function for charged particles of hard momentum in scalar QED. The goal is to understand the effects of infrared divergences associated with the exchange of quasistatic magnetic photons in the relaxation of the distribution function. We begin by obtaining a kinetic transport equation for the distribution function for hard charged scalars in a perturbative expansion that includes hard thermal loop resummation. Solving this transport equation, the infrared divergences arising from absorption and emission of soft quasi-static magnetic photons are manifest in logarithmic secular terms. We then implement the dynamical renormalization group resummation of these secular terms in the relaxation time approximation. The distribution function (in the linearized regime) is found to approach equilibrium as δnk(t)=δnk(to)e2αT(tto)ln[(tto)μˉ]\delta n_k(t) =\delta n_k(t_o) e^{-2\alpha T (t-t_o) \ln[(t-t_o)\bar{\mu}]}, with μˉωp\bar{\mu}\approx \omega_p the plasma frequency and α=e2/4π\alpha =e^2/4\pi. This anomalous relaxation is recognized to be the square of the relaxation of the single particle propagator, providing a generalization of the usual relation between the damping and the interaction rate. The renormalization group approach to kinetics reveals clearly the time scale trel(αTln[1/α])1t_{rel} \approx (\alpha T \ln[1/\alpha])^{-1} arising from infrared physics and hinges upon the separation of scales trel>>ωp1t_{rel} >>\omega_p^{-1}.Comment: 16 pages, no figure
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