Phase diagram of orbital-selective Mott transitions at finite temperatures

Mott transitions in the two-orbital Hubbard model with different bandwidths are investigated at finite temperatures. By means of the self-energy functional approach, we discuss the stability of the intermediate phase with one orbital localized and the other itinerant, which is caused by the orbital-selective Mott transition (OSMT). It is shown that the OSMT realizes two different coexistence regions at finite temperatures in accordance with the recent results of Liebsch. We further find that the particularly interesting behavior emerges around the special condition $U=U'$ and J=0, which includes a new type of the coexistence region with three distinct states. By systematically changing the Hund coupling, we establish the global phase diagram to elucidate the key role played by the Hund coupling on the Mott transitions.Comment: 4 pages, 6 figure

Observational evidence for self-interacting cold dark matter

Cosmological models with cold dark matter composed of weakly interacting particles predict overly dense cores in the centers of galaxies and clusters and an overly large number of halos within the Local Group compared to actual observations. We propose that the conflict can be resolved if the cold dark matter particles are self-interacting with a large scattering cross-section but negligible annihilation or dissipation. In this scenario, astronomical observations may enable us to study dark matter properties that are inaccessible in the laboratoryComment: 4 pages, no figures; added references, pedagogical improvements, to appear in PR

Linear and non-linear perturbations in dark energy models

I review the linear and second-order perturbation theory in dark energy models with explicit interaction to matter in view of applications to N-body simulations and non-linear phenomena. Several new or generalized results are obtained: the general equations for the linear perturbation growth; an analytical expression for the bias induced by a species-dependent interaction; the Yukawa correction to the gravitational potential due to dark energy interaction; the second-order perturbation equations in coupled dark energy and their Newtonian limit. I also show that a density-dependent effective dark energy mass arises if the dark energy coupling is varying.Comment: 12 pages, submitted to Phys. Rev; v2: added a ref. and corrected a typ

Defense styles from the perspective of affective neuroscience

To our knowledge, no study has been carried out to observe which subcortical basic affective systems are related to which defense styles. Such a perspective may have the potential to reveal how defenses may interact with subcortical primary emotional systems (PES) and how they contribute to affect regulation. We aimed to analyze the relationship of immature, neurotic, and mature defenses with basic subcortical affects (CARE, PLAY, SEEK, SADNESS, FEAR, ANGER) within an affective neuroscientific perspective. In addition, we sought to explore the effect of psychiatric disorders in relation to PES and defenses, and observe gender effects, if any. The sample consisted of 703 university students, recruited online. The materials included the Turkish translations of the Affective Neuroscience Personality Scales (ANPS) and the Defense Style Questionnaire (DSQ). The correlations between ANPS and DSQ showed that the immature defenses increase as all negative emotions increase, whereas mature defenses increase as all positive emotions (except CARE) increase and all negative affects decrease (except ANGER). On the other hand, as neurotic defenses increase, CARE, FEAR and SADNESS simultaneously increase. Subjects who reported the presence of psychiatric disorders also reported higher FEAR, SADNESS, ANGER accompanied by higher immature defenses. Finally, male subjects reported higher immature defenses, whereas the females reported higher neurotic defenses, accompanied by higher CARE, SEEK, SADNESS, FEAR, and slightly lower PLAY. Investigating defenses through the lens of affective neuroscience offers the opportunity to link the abstract concept of defenses to increasingly well-understood neurobiology

The Chromatin Modifier MSK1/2 Suppresses Endocrine Cell Fates during Mouse Pancreatic Development

Type I diabetes is caused by loss of insulin-secreting beta cells. To identify novel, pharmacologically-targetable histone-modifying proteins that enhance beta cell production from pancreatic progenitors, we performed a screen for histone modifications induced by signal transduction pathways at key pancreatic genes. The screen led us to investigate the temporal dynamics of ser-28 phosphorylated histone H3 (H3S28ph) and its upstream kinases, MSK1 and MSK2 (MSK1/2). H3S28ph and MSK1/2 were enriched at the key endocrine and acinar promoters in E12.5 multipotent pancreatic progenitors. Pharmacological inhibition of MSK1/2 in embryonic pancreatic explants promoted the specification of endocrine fates, including the beta-cell lineage, while depleting acinar fates. Germline knockout of both Msk isoforms caused enhancement of alpha cells and a reduction in acinar differentiation, while monoallelic loss of Msk1 promoted beta cell mass. Our screen of chromatin state dynamics can be applied to other developmental contexts to reveal new pathways and approaches to modulate cell fates

The developmental regulator Pax6 is essential for maintenance of islet cell function in the adult mouse pancreas

The transcription factor Pax6 is a developmental regulator with a crucial role in development of the eye, brain, and olfactory system. Pax6 is also required for correct development of the endocrine pancreas and specification of hormone producing endocrine cell types. Glucagon-producing cells are almost completely lost in Pax6-null embryos, and insulin-expressing beta and somatostatin-expressing delta cells are reduced. While the developmental role of Pax6 is well-established, investigation of a further role for Pax6 in the maintenance of adult pancreatic function is normally precluded due to neonatal lethality of Pax6-null mice. Here a tamoxifen-inducible ubiquitous Cre transgene was used to inactivate Pax6 at 6 months of age in a conditional mouse model to assess the effect of losing Pax6 function in adulthood. The effect on glucose homeostasis and the expression of key islet cell markers was measured. Homozygous Pax6 deletion mice, but not controls, presented with all the symptoms of classical diabetes leading to severe weight loss requiring termination of the experiment five weeks after first tamoxifen administration. Immunohistochemical analysis of the pancreata revealed almost complete loss of Pax6 and much reduced expression of insulin, glucagon, and somatostatin. Several other markers of islet cell function were also affected. Notably, strong upregulation in the number of ghrelin-expressing endocrine cells was observed. These findings demonstrate that Pax6 is essential for adult maintenance of glucose homeostasis and function of the endocrine pancreas

The Lantern Vol. 18, No. 3, Spring 1950

• The Rise and Fall of Mr. Fluff • Thoughts by the Sea • Equality of Men • On Radio Comedians • After Hours • Rain • Morning • Escape from Fear • Book of Red • Poems by a Guy Named Mike • We are the People • Spirit Disrupted • Light • Sonnethttps://digitalcommons.ursinus.edu/lantern/1051/thumbnail.jp

Musashi expression in β-cells coordinates insulin expression, apoptosis and proliferation in response to endoplasmic reticulum stress in diabetes

Diabetes is associated with the death and dysfunction of insulin-producing pancreatic β-cells. In other systems, Musashi genes regulate cell fate via Notch signaling, which we recently showed regulates β-cell survival. Here we show for the first time that human and mouse adult islet cells express mRNA and protein of both Musashi isoforms, as well Numb/Notch/Hes/neurogenin-3 pathway components. Musashi expression was observed in insulin/glucagon double-positive cells during human fetal development and increased during directed differentiation of human embryonic stem cells (hESCs) to the pancreatic lineage. De-differentiation of β-cells with activin A increased Msi1 expression. Endoplasmic reticulum (ER) stress increased Msi2 and Hes1, while it decreased Ins1 and Ins2 expression, revealing a molecular link between ER stress and β-cell dedifferentiation in type 2 diabetes. These effects were independent of changes in Numb protein levels and Notch activation. Overexpression of MSI1 was sufficient to increase Hes1, stimulate proliferation, inhibit apoptosis and reduce insulin expression, whereas Msi1 knockdown had the converse effects on proliferation and insulin expression. Overexpression of MSI2 resulted in a decrease in MSI1 expression. Taken together, these results demonstrate overlapping, but distinct roles for Musashi-1 and Musashi-2 in the control of insulin expression and β-cell proliferation. Our data also suggest that Musashi is a novel link between ER stress and the compensatory β-cell proliferation and the loss of β-cell gene expression seen in specific phases of the progression to type 2 diabetes

Pdx1 and Ngn3 Overexpression Enhances Pancreatic Differentiation of Mouse ES Cell-Derived Endoderm Population

In order to define the molecular mechanisms regulating the specification and differentiation of pancreatic β-islet cells, we investigated the effect of upregulating Pdx1 and Ngn3 during the differentiation of the β-islet-like cells from murine embryonic stem (ES) cell-derived activin induced-endoderm. Induced overexpression of Pdx1 resulted in a significant upregulation of insulin (Ins1 and Ins2), and other pancreas-related genes. To enhance the developmental progression from the pancreatic bud to the formation of the endocrine lineages, we induced the overexpression express of Ngn3 together with Pdx1. This combination dramatically increased the level and timing of maximal Ins1 mRNA expression to approximately 100% of that found in the βTC6 insulinoma cell line. Insulin protein and C-peptide expression was confirmed by immunohistochemistry staining. These inductive effects were restricted to c-kit+ endoderm enriched EB-derived populations suggesting that Pdx1/Ngn3 functions after the specification of pancreatic endoderm. Although insulin secretion was stimulated by various insulin secretagogues, these cells had only limited glucose response. Microarray analysis was used to evaluate the expression of a broad spectrum of pancreatic endocrine cell-related genes as well as genes associated with glucose responses. Taken together, these findings demonstrate the utility of manipulating Pdx1 and Ngn3 expression in a stage-specific manner as an important new strategy for the efficient generation of functionally immature insulin-producing β-islet cells from ES cells