Large Scale Structure Formation with Global Topological Defects. A new Formalism and its implementation by numerical simulations

We investigate cosmological structure formation seeded by topological defects which may form during a phase transition in the early universe. First we derive a partially new, local and gauge invariant system of perturbation equations to treat microwave background and dark matter fluctuations induced by topological defects or any other type of seeds. We then show that this system is well suited for numerical analysis of structure formation by applying it to seeds induced by fluctuations of a global scalar field. Our numerical results are complementary to previous investigations since we use substantially different methods. The resulting microwave background fluctuations are compatible with older simulations. We also obtain a scale invariant spectrum of fluctuations with about the same amplitude. However, our dark matter results yield a smaller bias parameter compatible with $b\sim 2$ on a scale of $20 Mpc$ in contrast to previous work which yielded to large bias factors. Our conclusions are thus more positive. According to the aspects analyzed in this work, global topological defect induced fluctuations yield viable scenarios of structure formation and do better than standard CDM on large scales.Comment: uuencoded, compressed tar-file containing the text in LaTeX and 12 Postscript Figures, 41 page

Tension between SN and BAO: current status and future forecasts

Using real and synthetic Type Ia SNe (SNeIa) and baryon acoustic oscillations (BAO) data representing current observations forecasts, this paper investigates the tension between those probes in the dark energy equation of state (EoS) reconstruction considering the well known CPL model and Wang's low correlation reformulation. In particular, here we present simulations of BAO data from both the the radial and transverse directions. We also explore the influence of priors on Omega_m and Omega_b on the tension issue, by considering 1-sigma deviations in either one or both of them. Our results indicate that for some priors there is no tension between a single dataset (either SNeIa or BAO) and their combination (SNeIa+BAO). Our criterion to discern the existence of tension (sigma-distance) is also useful to establish which is the dataset with most constraining power; in this respect SNeIa and BAO data switch roles when current and future data are considered, as forecasts predict and spectacular quality improvement on BAO data. We also find that the results on the tension are blind to the way the CPL model is addressed: there is a perfect match between the original formulation and that by the low correlation optimized, but the errors on the parameters are much narrower in all cases of our exhaustive exploration, thus serving the purpose of stressing the convenience of this reparametrization.Comment: 21 pages, under review in JCA

Maternal Choline Supplementation Alters Basal Forebrain Cholinergic Neuron Gene Expression In The Ts65Dn Mouse Model Of Down Syndrome

Down syndrome (DS), trisomy 21, is marked by intellectual disability and a premature aging profile including degeneration of the basal forebrain cholinergic neuron (BFCN) projection system, similar to Alzheimer\u27s disease (AD). Although data indicate that perinatal maternal choline supplementation (MCS) alters the structure and function of these neurons in the Ts65Dn mouse model of DS and AD (Ts), whether MCS affects the molecular profile of vulnerable BFCNs remains unknown. We investigated the genetic signature of BFCNs obtained from Ts and disomic (2N) offspring of Ts65Dn dams maintained on a MCS diet (Ts+, 2N+) or a choline normal diet (ND) from mating until weaning, then maintained on ND until 4.4–7.5 months of age. Brains were then collected and prepared for choline acetyltransferase (ChAT) immunohistochemistry and laser capture microdissection followed by RNA extraction and custom-designed microarray analysis. Findings revealed upregulation of select transcripts in classes of genes related to the cytoskeleton (Tubb4b), AD (Cav1), cell death (Bcl2), presynaptic (Syngr1), immediate early (Fosb, Arc), G protein signaling (Gabarap, Rgs10), and cholinergic neurotransmission (Chrnb3) in Ts compared to 2N mice, which were normalized with MCS. Moreover, significant downregulation was seen in select transcripts associated with the cytoskeleton (Dync1h1), intracellular signaling (Itpka, Gng3, and Mlst8), and cell death (Ccng1) in Ts compared to 2N mice that was normalized with MCS. This study provides insight into genotype-dependent differences and the effects of MCS at the molecular level within a key vulnerable cell type in DS and AD