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Insoluble particles in ice cores record signatures of past climate parameters like vegetation, volcanic activity or aridity. Their analytical detection depends on intensive bench microscopy investigation and requires dedicated sample preparation steps. Both are laborious, require in-depth knowledge and often restrict sampling strategies. To help overcome these limitations, we present a framework based on Flow Imaging Microscopy coupled to a deep neural network for autonomous image classification of ice core particles. We train the network to classify 7 commonly found classes: mineral dust, felsic and basaltic volcanic ash (tephra), three species of pollen (Corylus avellana, Quercus robur, Quercus suber) and contamination particles that may be introduced onto the ice core surface during core handling operations. The trained network achieves 96.8 % classification accuracy at test time. We present the system’s potentials and limitations with respect to the detection of mineral dust, pollen grains and tephra shards, using both controlled materials and real ice core samples. The methodology requires little sample material, is non destructive, fully reproducible and does not require any sample preparation step. The presented framework can bolster research in the field, by cutting down processing time, supporting human-operated microscopy and further unlocking the paleoclimate potential of ice core records by providing the opportunity to identify an array of ice core particles. Suggestions for an improved system to be deployed within a continuous flow analysis workflow are also presented. [ABSTRACT FROM AUTHOR]

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2009.05.569 Byline: Katherine Whalley, Stefanie Gogel, Sigrun Lange, Patrizia Ferretti Keywords: Chick; Development; Doublecortin; Glast; Injury; Neurogenesis; NeuN; Radial glia; Regeneration; Spinal cord; Transitin Abstract: The chick spinal cord can regenerate following injury until advanced developmental stages. It is conceivable that changes in stem/progenitor cell plasticity contribute to the loss of this capacity, which occurs around E13. We investigated the contribution of proliferation, phenotypic changes in radial glia progenitors, and neurogenesis to spinal cord regeneration. There was no early up-regulation of markers of gliogenic radial glia after injury either at E11 or E15. In contrast, increased proliferation in the grey matter and up-regulation of transitin expression following injury at E11, but not E15, suggested high levels of plasticity within the E11 spinal cord progenitor population that are lost by later stages. Changes in neural progenitors with development were also supported by a higher neurosphere forming ability at E11 than at E15. Co-labelling with doublecortin and neuron-specific markers and BrdU in spinal cord sections and dissociated cells showed that neurogenesis is an ongoing process in E11 chick spinal cords. This neurogenesis appeared to be complete by E15. Our findings demonstrate that the regeneration-competent chick spinal cord is less mature and more plastic than previously believed, which may contribute to its favourable response to injury, and suggest a role for neurogenesis in maintaining regenerative capacity. Author Affiliation: Developmental Biology Unit, UCL Institute of Child Health, 30 Guilford Street, London WC1N 1EH, UK Article History: Received 7 November 2008; Revised 26 May 2009; Accepted 27 May 2009

Author(s): Aradhna Tripati (corresponding author) [1]; Jan Backman [2]; Henry Elderfield [1]; Patrizia Ferretti [1] A change in the state of Earth's ocean-climate system occurred at the end of the [...]

Normal growth and morphogenesis of the cranial vault reflect a balance between cell proliferation in the sutures and osteogenesis at the margins of the cranial bones. In the clinical condition craniosynostosis, the sutures fuse prematurely as a result of precocious osteogenic differentiation and craniofacial malformation results. Mutations in several fibroblast growth factor receptor (FGFR) genes have now been identified as being responsible for the major craniosynostotic syndromes. We have used a grafting technique to manipulate the levels of endogenous FGF-2 ligand in embryonic chick cranial vaults and thereby perturb morphogenesis. Implantation of beads loaded with FGF-2 did not affect normal cranial development at physiological concentrations, although they elicited a morphogenetic response in the limb. Implantation of beads loaded with a neutralising antibody to FGF-2 generated a concentration-dependent response. When a single bead was implanted, the grafts grew to a massive size as a result of increased cell division in the tissue. With greater inactivation of FGF-2 protein (two to three beads implanted), all further bone differentiation and cell proliferation was blocked. These data further support the emerging idea that the intensity of FGF-mediated signalling determines the developmental fate of the skeletogenic cells in the cranial vault. High and low levels correlate with differentiation and proliferation, respectively. A balance between the two ensures normal cranial vault morphogenesis. This is consistent with the observation that several FGFR mutations causing craniosynostosis result in constitutive activation of the receptor. Key Words: neural crest; osteogenesis; FGF-2; cranium; suture.