The Chemical Composition of Carbon-Rich, Very Metal-Poor Stars: A New Class of Mildly Carbon-Rich Objects Without Excess of Neutron-Capture Elements

We report on an analysis of the chemical composition of five carbon-rich, very metal-poor stars based on high-resolution spectra. One star, CS22948-027, exhibits very large overabundances of carbon, nitrogen, and the neutron-capture elements, as found in the previous study of Hill et al.. This result may be interpreted as a consequence of mass transfer from a binary companion that previously evolved through the asymptotic giant branch stage. By way of contrast, the other four stars we investigate exhibit no overabundances of barium ([Ba/Fe]<0), while three of them have mildly enhanced carbon and/or nitrogen ([C+N]+1). We have been unable to determine accurate carbon and nitrogen abundances for the remaining star (CS30312-100). These stars are rather similar to the carbon-rich, neutron-capture-element-poor star CS22957-027 discussed previously by Norris et al., though the carbon overabundance in this object is significantly larger ([C/Fe]=+2.2). Our results imply that these carbon-rich objects with ``normal'' neutron-capture element abundances are not rare among very metal-deficient stars. One possible process to explain this phenomenon is as a result of helium shell flashes near the base of the AGB in very low-metallicity, low-mass (M~< 1M_sun) stars, as recently proposed by Fujimoto et al.. The moderate carbon enhancements reported herein ([C/Fe]+1) are similar to those reported in the famous r-process-enhanced star CS22892-052. We discuss the possibility that the same process might be responsible for this similarity, as well as the implication that a completely independent phenomenon was responsible for the large r-process enhancement in CS22892-052.Comment: 53 pages, 8 figures, to appear in Ap

A computational procedure for functional characterization of potential marker genes from molecular data: Alzheimer's as a case study

Abstract Background A molecular characterization of Alzheimer's Disease (AD) is the key to the identification of altered gene sets that lead to AD progression. We rely on the assumption that candidate marker genes for a given disease belong to specific pathogenic pathways, and we aim at unveiling those pathways stable across tissues, treatments and measurement systems. In this context, we analyzed three heterogeneous datasets, two microarray gene expression sets and one protein abundance set, applying a recently proposed feature selection method based on regularization. Results For each dataset we identified a signature that was successively evaluated both from the computational and functional characterization viewpoints, estimating the classification error and retrieving the most relevant biological knowledge from different repositories. Each signature includes genes already known to be related to AD and genes that are likely to be involved in the pathogenesis or in the disease progression. The integrated analysis revealed a meaningful overlap at the functional level. Conclusions The identification of three gene signatures showing a relevant overlap of pathways and ontologies, increases the likelihood of finding potential marker genes for AD.</p

Enhanced Functional Recovery in MRL/MpJ Mice after Spinal Cord Dorsal Hemisection

Adult MRL/MpJ mice have been shown to possess unique regeneration capabilities. They are able to heal an ear-punched hole or an injured heart with normal tissue architecture and without scar formation. Here we present functional and histological evidence for enhanced recovery following spinal cord injury (SCI) in MRL/MpJ mice. A control group (C57BL/6 mice) and MRL/MpJ mice underwent a dorsal hemisection at T9 (thoracic vertebra 9). Our data show that MRL/MpJ mice recovered motor function significantly faster and more completely. We observed enhanced regeneration of the corticospinal tract (CST). Furthermore, we observed a reduced astrocytic response and fewer micro-cavities at the injury site, which appear to create a more growth-permissive environment for the injured axons. Our data suggest that the reduced astrocytic response is in part due to a lower lesion-induced increase of cell proliferation post-SCI, and a reduced astrocytic differentiation of the proliferating cells. Interestingly, we also found an increased number of proliferating microglia, which could be involved in the MRL/MpJ spinal cord repair mechanisms. Finally, to evaluate the molecular basis of faster spinal cord repair, we examined the difference in gene expression changes in MRL/MpJ and C57BL/6 mice after SCI. Our microarray data support our histological findings and reveal a transcriptional profile associated with a more efficient spinal cord repair in MRL/MpJ mice