Scaling Limits of Processes with Fast Nonlinear Mean Reversion

We derive scaling limits for integral functionals of It\^o processes with fast nonlinear mean-reversion speed. We show that in these limits, the fast mean-reverting process is "averaged out" by integrating against its invariant measure. These convergence results hold uniformly in probability and, under mild integrability conditions, also in $\mathcal{S}^p$. They are a crucial building block for the analysis of portfolio choice models with small superlinear transaction costs, carried out in the companion paper of the present study.Comment: 37 pages, no figur

Destruction of molecular compounds in gaseous and liquid medium in microwave discharge plasma

The paper presents the results of experimental studies of molecular destruction in gaseous and liquid medium using microwave discharge plasma at atmospheric pressure. As the gas medium hydrocarbon gas is used, the liquid medium were aqueous solutions of methylene blue and more complex organic compound in the form of humic substances. As a result of the destruction of hydrocarbon gas molecules in microwave discharge plasma new products such as hydrogen, ethylene, acetylene and carbon nanostructured material have been formed. In experiments on destruction of molecular compounds in aqueous organic solutions we used air, nitrogen and argon for plasma gases. It is shown that the process of molecular destruction in aqueous organic solutions in the microwave discharge plasma is based on oxidation-reduction reactions. It is found that the maximum efficiency of removal of organic compounds from the solution occurs when using air as the plasma gas

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

A method to measure the resonance transitions between the gravitationally bound quantum states of neutrons in the GRANIT spectrometer

We present a method to measure the resonance transitions between the gravitationally bound quantum states of neutrons in the GRANIT spectrometer. The purpose of GRANIT is to improve the accuracy of measurement of the quantum states parameters by several orders of magnitude, taking advantage of long storage of Ultracold neutrons at specula trajectories. The transitions could be excited using a periodic spatial variation of a magnetic field gradient. If the frequency of such a perturbation (in the frame of a moving neutron) coincides with a resonance frequency defined by the energy difference of two quantum states, the transition probability will sharply increase. The GRANIT experiment is motivated by searches for short-range interactions (in particular spin-dependent interactions), by studying the interaction of a quantum system with a gravitational field, by searches for extensions of the Standard model, by the unique possibility to check the equivalence principle for an object in a quantum state and by studying various quantum optics phenomena

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