Multiwavelength Study on Solar and Interplanetary Origins of the Strongest Geomagnetic Storm of Solar Cycle 23

We study the solar sources of an intense geomagnetic storm of solar cycle 23 that occurred on 20 November 2003, based on ground- and space-based multiwavelength observations. The coronal mass ejections (CMEs) responsible for the above geomagnetic storm originated from the super-active region NOAA 10501. We investigate the H-alpha observations of the flare events made with a 15 cm solar tower telescope at ARIES, Nainital, India. The propagation characteristics of the CMEs have been derived from the three-dimensional images of the solar wind (i.e., density and speed) obtained from the interplanetary scintillation data, supplemented with other ground- and space-based measurements. The TRACE, SXI and H-alpha observations revealed two successive ejections (of speeds ~350 and ~100 km/s), originating from the same filament channel, which were associated with two high speed CMEs (~1223 and ~1660 km/s, respectively). These two ejections generated propagating fast shock waves (i.e., fast drifting type II radio bursts) in the corona. The interaction of these CMEs along the Sun-Earth line has led to the severity of the storm. According to our investigation, the interplanetary medium consisted of two merging magnetic clouds (MCs) that preserved their identity during their propagation. These magnetic clouds made the interplanetary magnetic field (IMF) southward for a long time, which reconnected with the geomagnetic field, resulting the super-storm (Dst_peak=-472 nT) on the Earth.Comment: 24 pages, 16 figures, Accepted for publication in Solar Physic

Revising the embryonic origin of thyroid C cells in mice and humans.

Current understanding infers a neural crest origin of thyroid C cells, the major source of calcitonin in mammals and ancestors to neuroendocrine thyroid tumors. The concept is primarily based on investigations in quail–chick chimeras involving fate mapping of neural crest cells to the ultimobranchial glands that regulate Ca2+ homeostasis in birds, reptiles, amphibians and fishes, but whether mammalian C cell development involves a homologous ontogenetic trajectory has not been experimentally verified. With lineage tracing, we now provide direct evidence that Sox17+ anterior endoderm is the only source of differentiated C cells and their progenitors in mice. Like many gut endoderm derivatives, embryonic C cells were found to coexpress pioneer factors forkhead box (Fox) a1 and Foxa2 before neuroendocrine differentiation takes place. In the ultimobranchial body epithelium emerging from pharyngeal pouch endoderm in early organogenesis, differential Foxa1/Foxa2 expression distinguished two spatially separated pools of C cell precursors with different growth properties. A similar expression pattern was recapitulated in medullary thyroid carcinoma cells in vivo, consistent with a growth-promoting role of Foxa1. In contrast to embryonic precursor cells, C cell-derived tumor cells invading the stromal compartment downregulated Foxa2, foregoing epithelial-to-mesenchymal transition designated by loss of E-cadherin;bothFoxa2 andE-cadherinwere re-expressed atmetastatic sites. These findings revise mammalian C cell ontogeny, expand the neuroendocrine repertoire of endoderm and redefine the boundaries of neural crest diversification.The data further underpin distinct functions of Foxa1 and Foxa2 in both embryonic and tumor development