The fetal origins of the metabolic syndrome: Can we intervene?

Epidemiological studies have suggested that metabolic programming begins during fetal life and adverse events in utero are a critical factor in the etiology of chronic diseases and overall health. While the underlying molecular mechanisms linking impaired fetal development to these adult diseases are being elucidated, little is known about how we can intervene early in life to diminish the incidence and severity of these long-term diseases. This paper highlights the latest clinical and pharmaceutical studies addressing how dietary intervention in fetal and neonatal life may be able to prevent aspects of the metabolic syndrome associated with IUGR pregnancies. © 2012 Noelle Ma and Daniel B. Hardy

Complex critical exponents for percolation transitions in Josephson-junction arrays, antiferromagnets, and interacting bosons

We show that the critical behavior of quantum systems undergoing a percolation transition is dramatically affected by their topological Berry phase $2\pi\rho$. For irrational $\rho$, we demonstrate that the low-energy excitations of diluted Josephson-junctions arrays, quantum antiferromagnets, and interacting bosons are spinless fermions with fractal spectrum. As a result, critical properties not captured by the usual Ginzburg-Landau-Wilson description of phase transitions emerge, such as complex critical exponents, log-periodic oscillations and dynamically broken scale-invariance.Comment: revised version accepted for publication in Phys. Rev. Let

Defining the chromatin signature of inducible genes in T cells

BACKGROUND Specific chromatin characteristics, especially the modification status of the core histone proteins, are associated with active and inactive genes. There is growing evidence that genes that respond to environmental or developmental signals may possess distinct chromatin marks. Using a T cell model and both genome-wide and gene-focused approaches, we examined the chromatin characteristics of genes that respond to T cell activation. RESULTS To facilitate comparison of genes with similar basal expression levels, we used expression-profiling data to bin genes according to their basal expression levels. We found that inducible genes in the lower basal expression bins, especially rapidly induced primary response genes, were more likely than their non-responsive counterparts to display the histone modifications of active genes, have RNA polymerase II (Pol II) at their promoters and show evidence of ongoing basal elongation. There was little or no evidence for the presence of active chromatin marks in the absence of promoter Pol II on these inducible genes. In addition, we identified a subgroup of genes with active promoter chromatin marks and promoter Pol II but no evidence of elongation. Following T cell activation, we find little evidence for a major shift in the active chromatin signature around inducible gene promoters but many genes recruit more Pol II and show increased evidence of elongation. CONCLUSIONS These results suggest that the majority of inducible genes are primed for activation by having an active chromatin signature and promoter Pol II with or without ongoing elongation

Local cloning of entangled states

We investigate the conditions under which a set \SC of pure bipartite quantum states on a $D\times D$ system can be locally cloned deterministically by separable operations, when at least one of the states is full Schmidt rank. We allow for the possibility of cloning using a resource state that is less than maximally entangled. Our results include that: (i) all states in \SC must be full Schmidt rank and equally entangled under the $G$-concurrence measure, and (ii) the set \SC can be extended to a larger clonable set generated by a finite group $G$ of order $|G|=N$, the number of states in the larger set. It is then shown that any local cloning apparatus is capable of cloning a number of states that divides $D$ exactly. We provide a complete solution for two central problems in local cloning, giving necessary and sufficient conditions for (i) when a set of maximally entangled states can be locally cloned, valid for all $D$; and (ii) local cloning of entangled qubit states with non-vanishing entanglement. In both of these cases, a maximally entangled resource is necessary and sufficient, and the states must be related to each other by local unitary "shift" operations. These shifts are determined by the group structure, so need not be simple cyclic permutations. Assuming this shifted form and partially entangled states, then in D=3 we show that a maximally entangled resource is again necessary and sufficient, while for higher dimensional systems, we find that the resource state must be strictly more entangled than the states in \SC. All of our necessary conditions for separable operations are also necessary conditions for LOCC, since the latter is a proper subset of the former. In fact, all our results hold for LOCC, as our sufficient conditions are demonstrated for LOCC, directly.Comment: REVTEX 15 pages, 1 figure, minor modifications. Same as the published version. Any comments are welcome

Maternal protein restriction leads to enhanced hepatic gluconeogenic gene expression in adult male rat offspring due to impaired expression of the liver x receptor

Epidemiological studies demonstrate that the link between impaired fetal development and glucose intolerance in later life is exacerbated by postnatal catch-up growth. Maternal protein restriction (MPR) during pregnancy and lactation in the rat has been previously demonstrated to lead to impaired glucose tolerance in adulthood, however the effects of protein restoration during weaning on glucose homeostasis are largely unknown. Recent in vitro studies have identified that the liver X receptor α(LXRα) maintains glucose homeostasis by inhibiting critical genes involved in gluconeogenesis including G6pase (G6pc), 11β-Hsd1 (Hsd11b1) and Pepck (Pck1). Therefore, we hypothesized that MPR with postnatal catch-up growth would impair LXRα in vivo, which in turn would lead to augmented gluconeogenic LXRα-target gene expression and glucose intolerance. To examine this hypothesis, pregnant Wistar rats were fed a control (20%) protein diet (C) or a low (8%) protein diet during pregnancy and switched to a control diet at birth (LP). At 4 months, the LP offspring had impaired glucose tolerance. In addition, LP offspring had decreased LXRα expression, while hepatic expression of 11β-HSD1 and G6Pase was significantly higher. This was concomitant with decreased binding of LXRα to the putative LXRE on 11β-Hsd1 and G6pase. Finally,we demonstrated that the acetylation of histone H3 (K9,14) surrounding the transcriptional start site of hepatic Lxrα (Nr1h3) was decreased in LP offspring, suggesting MPR-induced epigenetic silencing of the Lxrα promoter. In summary, our study demonstrates for the first time the important role of LXRα in mediating enhanced hepatic gluconeogenic gene expression and consequent glucose intolerance in adult MPR offspring. © 2013 Society for Endocrinology

Microwave properties of (PrxY1−x)Ba2Cu3O7−δ(Pr_xY_{1-x})Ba_2Cu_3O_{7-\delta} : Influence of magnetic scattering

We report measurements of the surface impedance $Z_s=R_s+iX_s$ of $(Pr_xY_{1-x})Ba_2Cu_3O_{7-\delta}$, $(x=0,0.15,0.23,0.3,0.4,0.5)$. Increasing $Pr$ concentration leads to some striking results not observed in samples doped by non-magnetic constituents. The three principal features of the $R_s(T)$ data - multiple structure in the transition, a high residual resistance and, at high $Pr$ concentrations, an upturn of the low $T$ data, are all characteristic of the influence of magnetic scattering on superconductivity, and appear to be common to materials where magnetism and superconductivity coexist. The low $T$ behavior of $\lambda (T)$ appears to change from $T$ to $T^4$ at large $Pr$ doping, and provides evidence of the influence of magnetic pairbreaking of the $Pr$.Comment: 5 pages, 3 eps figures, Revtex, 2-column format, uses graphicx. To appear in Physica C. Postscript version also available at http://sagar.physics.neu.edu/preprints.htm

Enhancement of superconducting transition temperature by the additional second neighbor hopping t' in the t-J model

Within the kinetic energy driven superconducting mechanism, the effect of the additional second neighbor hopping t' on the superconducting state of the t-J model is discussed. It is shown that t' plays an important role in enhancing the superconducting transition temperature of the t-J model. It is also shown that the superconducting-state of cuprate superconductors is the conventional Bardeen-Cooper-Schrieffer like, so that the basic Bardeen-Cooper-Schrieffer formalism is still valid in quantitatively reproducing the doping dependence of the superconducting gap parameter and superconducting transition temperature, and electron spectral function at $(\pi,0)$ point, although the pairing mechanism is driven by the kinetic energy by exchanging dressed spin excitations.Comment: 8 pages, 4 figures, added discussions and references, accepted for publication in Physics Letters

Mixing of superconducting dx2−y2d_{x^2-y^2} state with s-wave states for different filling and temperature

We study the order parameter for mixed-symmetry states involving a major $d_{x^2-y^2}$ state and various minor s-wave states ($s$, $s_{xy}$, and $s_{x^2+y^2}$) for different filling and temperature for mixing angles 0 and $\pi/2$. We employ a two-dimensional tight-binding model incorporating second-neighbor hopping for tetragonal and orthorhombic lattice. There is mixing for the symmetric $s$ state both on tetragonal and orthorhombic lattice. The $s_{xy}$ state mixes with the $d_{x^2-y^2}$ state only on orthorhombic lattice. The $s_{x^2+y^2}$ state never mixes with the $d_{x^2-y^2}$ state. The temperature dependence of the order parameters is also studied.Comment: 10 pages, 9 figures, accepted in Physica

A Genome-wide gene-expression analysis and database in transgenic mice during development of amyloid or tau pathology

We provide microarray data comparing genome-wide differential expression and pathology throughout life in four lines of "amyloid" transgenic mice (mutant human APP, PSEN1, or APP/PSEN1) and "TAU" transgenic mice (mutant human MAPT gene). Microarray data were validated by qPCR and by comparison to human studies, including genome-wide association study (GWAS) hits. Immune gene expression correlated tightly with plaques whereas synaptic genes correlated negatively with neurofibrillary tangles. Network analysis of immune gene modules revealed six hub genes in hippocampus of amyloid mice, four in common with cortex. The hippocampal network in TAU mice was similar except that Trem2 had hub status only in amyloid mice. The cortical network of TAU mice was entirely different with more hub genes and few in common with the other networks, suggesting reasons for specificity of cortical dysfunction in FTDP17. This Resource opens up many areas for investigation. All data are available and searchable at http://www.mouseac.org