Dynamism in the solar core

Recent results of a mixed shell model heated asymmetrically by transient increases in nuclear burning indicate the transient generation of small hot spots inside the Sun somewhere between 0.1 and 0.2 solar radii. These hot bubbles are followed by a nonlinear differential equation system with finite amplitude non-homologous perturbations which is solved in a solar model. Our results show the possibility of a direct connection between the dynamic phenomena of the solar core and the atmospheric activity. Namely, an initial heating about DQ_0 ~ 10^{31}-10^{37} ergs can be enough for a bubble to reach the outer convective zone. Our calculations show that a hot bubble can arrive into subphotospheric regions with DQ_final ~ 10^{28} - 10^{34} ergs with a high speed, up to 10 km s-1, approaching the local sound speed. We point out that the developing sonic boom transforms the shock front into accelerated particle beam injected upwards into the top of loop carried out by the hot bubble above its forefront traveling from the solar interior. As a result, a new perspective arises to explain flare energetics. We show that the particle beams generated by energetic deep-origin hot bubbles in the subphotospheric layers have masses, energies, and chemical compositions in the observed range of solar chromospheric and coronal flares. It is shown how the emergence of a hot bubble into subphotospheric regions offers a natural mechanism that can generate both the eruption leading to the flare and the observed coronal magnetic topology for reconnection. We show a list of long-standing problems of solar physics that our model explains. We present some predictions for observations, some of which are planned to be realized in the near future.Comment: 44 pages, 20 figure

2ʹ-Deoxyadenosine 5ʹ-diphosphoribose is an endogenous TRPM2 superagonist

Transient receptor potential melastatin 2 (TRPM2) is a ligand-gated Ca2+-permeable nonselective cation channel. Whereas physiological stimuli, such as chemotactic agents, evoke controlled Ca2+ signals via TRPM2, pathophysiological stimuli such as reactive oxygen species and genotoxic stress result in prolonged TRPM2-mediated Ca2+ entry and, consequently, apoptosis. To date, adenosine 5'-diphosphoribose (ADPR) has been assumed to be the main agonist for TRPM2. Here we show that 2'-deoxy-ADPR was a significantly better TRPM2 agonist, inducing 10.4-fold higher whole-cell currents at saturation. Mechanistically, this increased activity was caused by a decreased rate of inactivation and higher average open probability. Using high-performance liquid chromatography (HPLC) and mass spectrometry, we detected endogenous 2'-deoxy-ADPR in Jurkat T lymphocytes. Consistently, cytosolic nicotinamide mononucleotide adenylyltransferase 2 (NMNAT-2) and nicotinamide adenine dinucleotide (NAD)-glycohydrolase CD38 sequentially catalyzed the synthesis of 2'-deoxy-ADPR from nicotinamide mononucleotide (NMN) and 2'-deoxy-ATP in vitro. Thus, 2'-deoxy-ADPR is an endogenous TRPM2 superagonist that may act as a cell signaling molecule

The Polarity Protein Scribble Regulates Myelination and Remyelination in the Central Nervous System

The development and regeneration of myelin by oligodendrocytes, the myelin-forming cells of the central nervous system (CNS), requires profound changes in cell shape that lead to myelin sheath initiation and formation. Here, we demonstrate a requirement for the basal polarity complex protein Scribble in CNS myelination and remyelination. Scribble is expressed throughout oligodendroglial development and is up-regulated in mature oligodendrocytes where it is localised to both developing and mature CNS myelin sheaths. Knockdown of Scribble expression in cultured oligodendroglia results in disrupted morphology and myelination initiation. When Scribble expression is conditionally eliminated in the myelinating glia of transgenic mice, myelin initiation in CNS is disrupted, both during development and following focal demyelination, and longitudinal extension of the myelin sheath is disrupted. At later stages of myelination, Scribble acts to negatively regulate myelin thickness whilst suppressing the extracellular signal-related kinase (ERK)/mitogen-activated protein kinase (MAP) kinase pathway, and localises to non-compact myelin flanking the node of Ranvier where it is required for paranodal axo-glial adhesion. These findings demonstrate an essential role for the evolutionarily-conserved regulators of intracellular polarity in myelination and remyelination