142 research outputs found
Global vs local Casimir effect
This paper continues the investigation of the Casimir effect with the use of
the algebraic formulation of quantum field theory in the initial value setting.
Basing on earlier papers by one of us (AH) we approximate the Dirichlet and
Neumann boundary conditions by simple interaction models whose nonlocality in
physical space is under strict control, but which at the same time are
admissible from the point of view of algebraic restrictions imposed on models
in the context of Casimir backreaction. The geometrical setting is that of the
original parallel plates. By scaling our models and taking appropriate limit we
approach the sharp boundary conditions in the limit. The global force is
analyzed in that limit. One finds in Neumann case that although the sharp
boundary interaction is recovered in the norm resolvent sense for each model
considered, the total force per area depends substantially on its choice and
diverges in the sharp boundary conditions limit. On the other hand the local
energy density outside the interaction region, which in the limit includes any
compact set outside the strict position of the plates, has a universal limit
corresponding to sharp conditions. This is what one should expect in general,
and the lack of this discrepancy in Dirichlet case is rather accidental. Our
discussion pins down its precise origin: the difference in the order in which
scaling limit and integration over the whole space is carried out.Comment: 32 pages, accepted for publication in Ann. H. Poincar
Gravitomagnetic Moments and Dynamics of Dirac's (spin 1/2) fermions in flat space-time Maxwellian Gravity
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
Continuous Spectrum of Automorphism Groups and the Infraparticle Problem
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
-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
JNK1 phosphorylation of SCG10 determines microtubule dynamics and axodendritic length
C-Jun NH2-terminal kinases (JNKs) are essential during brain development, when they regulate morphogenic changes involving cell movement and migration. In the adult, JNK determines neuronal cytoarchitecture. To help uncover the molecular effectors for JNKs in these events, we affinity purified JNK-interacting proteins from brain. This revealed that the stathmin family microtubule-destabilizing proteins SCG10, SCLIP, RB3, and RB3' interact tightly with JNK. Furthermore, SCG10 is also phosphorylated by JNK in vivo on sites that regulate its microtubule depolymerizing activity, serines 62 and 73. SCG10-S73 phosphorylation is significantly decreased in JNK1-/- cortex, indicating that JNK1 phosphorylates SCG10 in developing forebrain. JNK phosphorylation of SCG10 determines axodendritic length in cerebrocortical cultures, and JNK site-phosphorylated SCG10 colocalizes with active JNK in embryonic brain regions undergoing neurite elongation and migration. We demonstrate that inhibition of cytoplasmic JNK and expression of SCG10-62A/73A both inhibited fluorescent tubulin recovery after photobleaching. These data suggest that JNK1 is responsible for regulation of SCG10 depolymerizing activity and neurite elongation during brain development
JNK Isoforms Differentially Regulate Neurite Growth and Regeneration in Dopaminergic Neurons In Vitro
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
Activation of MAPK ERK in peripheral nerve after injury
BACKGROUND: Activation of extracellular signal-regulated protein kinase (ERK), a member of mitogen-activated protein kinase (MAPK) family, has been proposed to mediate neurite outgrowth-promoting effects of several neurotrophic factors in vitro. However, the precise activity of ERK during axonal regeneration in vivo remains unclear. Peripheral axotomy has been shown to activate ERK in the cell bodies of primary afferent neurons and associated satellite cells. Nevertheless, whether ERK is also activated in the axons and surrounded Schwann cells which also play a key role in the regeneration process has not been clarified. RESULTS: Phosphorylation of ERK in the sciatic nerve in several time-points after crush injury has been examined. Higher phosphorylation of ERK was observed in the proximal and distal nerve stumps compared to the contralateral intact nerve from one day to one month after crush. The activation of ERK was mainly localized in the axons of the proximal segments. In the distal segments, however, active ERK was predominantly found in Schwann cells forming Bungner's bands. CONCLUSION: The findings indicate that ERK is activated in both the proximal and distal nerve stumps following nerve injury. The role of activated ERK in Wallerian degeneration and subsequent regeneration in vivo remains to be elucidated
Infraparticles with superselected direction of motion in two-dimensional conformal field theory
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
Axonal Varicosity Density as an Index of Local Neuronal Interactions
Diffuse transmission is an important non-synaptic communication mode in the cerebral neocortex, in which neurotransmitters released from en passant varicosities interact with surrounding cells. In a previous study we have shown that the cholinergic axonal segments which were in the microproximity with dopaminergic fibers possessed a greater density of en passant varicosities compared to more distant segments, suggesting an activity-dependent level of en passant varicosities in the axonal zone of interaction. To further evaluate this plastic relationship, the density of cholinergic varicosities was quantified on fiber segments within the microproximity of activated or non-activated pyramidal cells of the prefrontal cortex (mPFC). Repetitive 14 days patterned visual stimulation paired with an electrical stimulation of the cholinergic fibers projecting to the mPFC from the HDB was performed to induce persistent axonal plastic changes. The c-Fos early gene immunoreactivity was used as a neuronal activity marker of layer V pyramidal cells, labelled with anti-glutamate transporter EAAC1. Cholinergic fibers were labeled with anti-ChAT (choline acetyltransferase) immunostaining. The density of ChAT+ varicosities on and the length of fiber segments within the 3 µm microproximity of c-Fos positive/negative pyramidal cells were evaluated on confocal images. More than 50% of the pyramidal cells in the mPFC were c-Fos immunoreactive. Density of ChAT+ varicosities was significantly increased within 3 µm vicinity of activated pyramidal cells (0.50±0.01 per µm of ChAT+ fiber length) compared to non-activated cells in this group (0.34±0.001; p≤0.05) or control rats (0.32±0.02; p≤0.05). Different types of stimulation (visual, HDB or visual/HDB) induced similar increase of the density of ChAT+ varicosities within microproximity of activated pyramidal cells. This study demonstrated at the subcellular level an activity-dependent enrichment of ChAT+ varicosities in the axonal zone of interaction with other neuronal elements
The JNK Inhibitor XG-102 Protects against TNBS-Induced Colitis
The c-Jun N-terminal kinase (JNK)-inhibiting peptide D-JNKI-1, syn. XG-102 was tested for its therapeutic potential in acute inflammatory bowel disease (IBD) in mice. Rectal instillation of the chemical irritant trinitrobenzene sulfonic acid (TNBS) provoked a dramatic acute inflammation in the colon of 7–9 weeks old mice. Coincident subcutaneous application of 100 µg/kg XG-102 significantly reduced the loss of body weight, rectal bleeding and diarrhoea. After 72 h, the end of the study, the colon was removed and immuno-histochemically analysed. XG-102 significantly reduced (i) pathological changes such as ulceration or crypt deformation, (ii) immune cell pathology such as infiltration and presence of CD3- and CD68-positive cells, (iii) the production of tumor necrosis factor (TNF)-α in colon tissue cultures from TNBS-treated mice, (iv) expression of Bim, Bax, FasL, p53, and activation of caspase 3, (v) complexation of JNK2 and Bim, and (vi) expression and activation of the JNK substrate and transcription factor c-Jun. A single application of subcutaneous XG-102 was at least as effective or even better depending on the outcome parameter as the daily oral application of sulfasalazine used for treatment of IBD
Regulation of Retention of FosB Intron 4 by PTB
One effect of stressors such as chronic drug administration is that sequence within the terminal exon of the transcription factor FosB is recognized as intronic and removed by alternative splicing. This results in an open-reading-frame shift that produces a translation stop codon and ultimately a truncated protein, termed ΔFosB. In vitro splicing assays with control and mutated transcripts generated from a fosB mini-gene construct indicated a CU-rich sequence at the 3′ end of intron 4 (I4) plays an important role in regulating fosB pre-mRNA splicing due to its binding of polypyrimidine tract binding protein (PTB). PTB binding to this sequence is dependent upon phosphorylation by protein kinase A and is blocked if the CU-rich sequence is mutated to a U-rich region. When this mutated fosB minigene is expressed in HeLa cells, the splicing efficiency of its product is increased compared to wild type. Moreover, transient transfection of PTB-1 in HeLa cells decreased the splicing efficiency of a wild type fosB minigene transcript. Depletion of PTB from nuclear extracts facilitated U2AF65 binding to wild type sequence in vitro, suggesting these proteins function in a dynamic equilibrium to modulate fosB pre-mRNA alternative splicing. These results demonstrate for the first time that phosphorylated PTB promotes intron retention and thereby silences the splicing of fosB I4
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