338 research outputs found

    On the assertion that PCT violation implies Lorentz non-invariance

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    Out of conviction or expediency, some current research programs take for granted that "PCT violation implies violation of Lorentz invariance". We point out that this claim is still on somewhat shaky ground. In fact, for many years there has been no strengthening of the evidence in this direction. However, using causal perturbation theory, we prove here that when starting with a local PCT-invariant interaction, PCT symmetry can be maintained in the process of renormalization.Comment: 13 page

    Does Quantum Mechanics Clash with the Equivalence Principle - and Does it Matter?

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    With an eye on developing a quantum theory of gravity, many physicists have recently searched for quantum challenges to the equivalence principle of general relativity. However, as historians and philosophers of science are well aware, the principle of equivalence is not so clear. When clarified, we think quantum tests of the equivalence principle won't yield much. The problem is that the clash/not-clash is either already evident or guaranteed not to exist. Nonetheless, this work does help teach us what it means for a theory to be geometric.Comment: 12 page

    Continuous Spectrum of Automorphism Groups and the Infraparticle Problem

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    This paper presents a general framework for a refined spectral analysis of a group of isometries acting on a Banach space, which extends the spectral theory of Arveson. The concept of continuous Arveson spectrum is introduced and the corresponding spectral subspace is defined. The absolutely continuous and singular-continuous parts of this spectrum are specified. Conditions are given, in terms of the transposed action of the group of isometries, which guarantee that the pure-point and continuous subspaces span the entire Banach space. In the case of a unitarily implemented group of automorphisms, acting on a CC^*-algebra, relations between the continuous spectrum of the automorphisms and the spectrum of the implementing group of unitaries are found. The group of spacetime translation automorphisms in quantum field theory is analyzed in detail. In particular, it is shown that the structure of its continuous spectrum is relevant to the problem of existence of (infra-)particles in a given theory.Comment: 31 pages, LaTeX. As appeared in Communications in Mathematical Physic

    Gravitomagnetic Moments and Dynamics of Dirac's (spin 1/2) fermions in flat space-time Maxwellian Gravity

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    The gravitational effects in the relativistic quantum mechanics are investigated in a relativistically derived version of Heaviside's speculative Gravity (in flat space-time) named here as Maxwellian Gravity. The standard Dirac's approach to the intrinsic spin in the fields of Maxwellian Gravity yields the gravitomagnetic moment of a Dirac (spin 1/2) particle exactly equals to its intrinsic spin. Violation of The Equivalence Principle (both at classical and quantum mechanical level) in the relativistic domain has also been reported in this work.Comment: 27 page

    Loss of ATF2 Function Leads to Cranial Motoneuron Degeneration during Embryonic Mouse Development

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    The AP-1 family transcription factor ATF2 is essential for development and tissue maintenance in mammals. In particular, ATF2 is highly expressed and activated in the brain and previous studies using mouse knockouts have confirmed its requirement in the cerebellum as well as in vestibular sense organs. Here we present the analysis of the requirement for ATF2 in CNS development in mouse embryos, specifically in the brainstem. We discovered that neuron-specific inactivation of ATF2 leads to significant loss of motoneurons of the hypoglossal, abducens and facial nuclei. While the generation of ATF2 mutant motoneurons appears normal during early development, they undergo caspase-dependent and independent cell death during later embryonic and foetal stages. The loss of these motoneurons correlates with increased levels of stress activated MAP kinases, JNK and p38, as well as aberrant accumulation of phosphorylated neurofilament proteins, NF-H and NF-M, known substrates for these kinases. This, together with other neuropathological phenotypes, including aberrant vacuolisation and lipid accumulation, indicates that deficiency in ATF2 leads to neurodegeneration of subsets of somatic and visceral motoneurons of the brainstem. It also confirms that ATF2 has a critical role in limiting the activities of stress kinases JNK and p38 which are potent inducers of cell death in the CNS

    Neuronal c-Jun is required for successful axonal regeneration, but the effects of phosphorylation of its N-terminus are moderate.

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    Although neural c-Jun is essential for successful peripheral nerve regeneration, the cellular basis of this effect and the impact of c-Jun activation are incompletely understood. In the current study, we explored the effects of neuron-selective c-Jun deletion, substitution of serine 63 and 73 phosphoacceptor sites with non-phosphorylatable alanine, and deletion of Jun N-terminal kinases 1, 2 and 3 in mouse facial nerve regeneration. Removal of the floxed c-jun gene in facial motoneurons using cre recombinase under control of a neuron-specific synapsin promoter (junΔS) abolished basal and injury-induced neuronal c-Jun immunoreactivity, as well as most of the molecular responses following facial axotomy. Absence of neuronal Jun reduced the speed of axonal regeneration following crush, and prevented most cut axons from reconnecting to their target, significantly reducing functional recovery. Despite blocking cell death, this was associated with a large number of shrunken neurons. Finally, junΔS mutants also had diminished astrocyte and microglial activation and T-cell influx, suggesting that these non-neuronal responses depend on the release of Jun-dependent signals from neighboring injured motoneurons. The effects of substituting serine 63 and 73 phosphoacceptor sites (junAA), or of global deletion of individual kinases responsible for N-terminal c-Jun phosphorylation were mild. junAA mutants showed decrease in neuronal cell size, a moderate reduction in post-axotomy CD44 levels and slightly increased astrogliosis. Deletion of Jun N-terminal kinase (JNK)1 or JNK3 showed delayed functional recovery; deletion of JNK3 also interfered with T-cell influx, and reduced CD44 levels. Deletion of JNK2 had no effect. Thus, neuronal c-Jun is needed in regeneration, but JNK phosphorylation of the N-terminus mostly appears to not be required for its function

    JNK Isoforms Differentially Regulate Neurite Growth and Regeneration in Dopaminergic Neurons In Vitro

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    Parkinson’s disease is characterized by selective and progressive loss of midbrain DAergic neurons (MDN) in the substantia nigra and degeneration of its nigrostriatal projections. Whereas the cellular pathophysiology has been closely linked to an activation of c-Jun N-terminal kinases (JNKs) and c-Jun, the involvement of JNKs in regenerative processes of the nigrostriatal pathway is controversially discussed. In our study, we utilized a mechanical scratch lesion paradigm of midbrain DAergic neurons in vitro and studied regenerative neuritic outgrowth. After a siRNA-mediated knockdown of each of the three JNK isoforms, we found that JNKs differentially regulate neurite regeneration. Knockdown of JNK3 resulted in the most prominent neurite outgrowth impairment. This effect was attenuated again by plasmid overexpression of JNK3. We also evaluated cell survival of the affected neurons at the scratch border. JNK3 was found to be also relevant for survival of MDN which were lesioned by the scratch. Our data suggest that JNK isoforms are involved in differential regulation of cell death and regeneration in MDN depending on their neurite integrity. JNK3 appears to be required for regeneration and survival in the case of an environment permissive for regeneration. Future therapeutic approaches for the DAergic system may thus require isoform specific targeting of these kinases

    Infraparticles with superselected direction of motion in two-dimensional conformal field theory

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    Particle aspects of two-dimensional conformal field theories are investigated, using methods from algebraic quantum field theory. The results include asymptotic completeness in terms of (counterparts of) Wigner particles in any vacuum representation and the existence of (counterparts of) infraparticles in any charged irreducible product representation of a given chiral conformal field theory. Moreover, an interesting interplay between the infraparticle's direction of motion and the superselection structure is demonstrated in a large class of examples. This phenomenon resembles the electron's momentum superselection expected in quantum electrodynamics.Comment: 34 pages, no figure. The final version is available under Open Access. CC-B
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