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

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

Rotation in the dynamic factor modeling of multivariate stationary time series

dynamic factor model, identifiability, polynomial division, moving-average, rotation criteria,