Solar dynamo model with nonlocal alpha-effect

The first results of the solar dynamo model that allows for the diamagnetic effect of inhomogeneous turbulence and the nonlocal alpha-effect due to the rise of magnetic loops are discussed. The nonlocal alpha-effect is not subject to the catastrophic quenching related to the conservation of magnetic helicity. Given the diamagnetic pumping, the magnetic fields are concentrated near the base of the convection zone, although the distributed-type model covers the entire thickness of the convection zone. The magnetic cycle period, the equatorial symmetry of the field, its meridional drift, and the polar-to-toroidal field ratio obtained in the model are in agreement with observations. There is also some disagreement with observations pointing the ways of improving the model.Comment: To appear in Astronomy Letters, 10 pages, 5 figure

The model of dynamo with small number of modes and magnetic activity of T Tauri stars

The model that describes operation of dynamo in fully convective stars is presented. It is based on representation of stellar magnetic field as a superposition of finite number of poloidal and toroidal free damping modes. In the frame of adopted low of stellar differential rotation we estimated minimal value of dynamo number D, starting from which generation of cyclic magnetic field in stars without radiative core is possible. We also derived expression for period of the cycle. It was found that dynamo cycles of fully convective stars and stars with thin convective envelopes differ in a qualitative way: 1) distribution of spots over latitude during the cycle is different in these stars; 2) the model predicts that spot formation in fully convective stars should be strongly suppressed at some phases of the cycle. We have analyzed historical lightcurve of WTTS star V410 Tau and found that long term activity of the star is not periodic process. Rather one can speak about quasi cyclic activity with characteristic time of $\sim 4$ yr and chaotic component over imposed. We concluded also that redistribution of cool spots over longitude is the reason of long term variations of V410 Tau brightness. It means that one can not compare directly results of photometric observations with predictions of our axially symmetric (for simplicity) model which allows to investigate time evolution of spot's distribution over latitude. We then discuss what kind of observations and in which way could be used to check predictions of the dynamo theory.Comment: 18 pages, 5 figures, accepted to Astron. Let

Interferon-α Abrogates Tolerance Induction by Human Tolerogenic Dendritic Cells

BACKGROUND: Administration of interferon-α (IFN-α) represents an approved adjuvant therapy as reported for malignancies like melanoma and several viral infections. In malignant diseases, tolerance processes are critically involved in tumor progression. In this study, the effect of IFN-α on tolerance induction by human tolerogenic dendritic cells (DC) was analyzed. We focussed on tolerogenic IL-10-modulated DC (IL-10 DC) that are known to induce anergic regulatory T cells (iTregs). METHODOLOGY/PRINCIPAL FINDINGS: IFN-α promoted an enhanced maturation of IL-10 DC as demonstrated by upregulation of the differentiation marker CD83 as well as costimulatory molecules. IFN-α treatment resulted in an increased capacity of DC to stimulate T cell activation compared to control tolerogenic DC. We observed a strengthened T cell proliferation and increased IFN-γ production of CD4(+) and CD8(+) T cells stimulated by IFN-α-DC, demonstrating a restoration of the immunogenic capacity of tolerogenic DC in the presence of IFN-α. Notably, restimulation experiments revealed that IFN-α treatment of tolerogenic DC abolished the induction of T cell anergy and suppressor function of iTregs. In contrast, IFN-α neither affected the priming of iTregs nor converted iTregs into effector T cells. CONCLUSIONS/SIGNIFICANCE: IFN-α inhibits the induction of T cell tolerance by reversing the tolerogenic function of human DC

Nonviral Approaches for Neuronal Delivery of Nucleic Acids

The delivery of therapeutic nucleic acids to neurons has the potential to treat neurological disease and spinal cord injury. While select viral vectors have shown promise as gene carriers to neurons, their potential as therapeutic agents is limited by their toxicity and immunogenicity, their broad tropism, and the cost of large-scale formulation. Nonviral vectors are an attractive alternative in that they offer improved safety profiles compared to viruses, are less expensive to produce, and can be targeted to specific neuronal subpopulations. However, most nonviral vectors suffer from significantly lower transfection efficiencies than neurotropic viruses, severely limiting their utility in neuron-targeted delivery applications. To realize the potential of nonviral delivery technology in neurons, vectors must be designed to overcome a series of extra- and intracellular barriers. In this article, we describe the challenges preventing successful nonviral delivery of nucleic acids to neurons and review strategies aimed at overcoming these challenges