Cosmology of hidden sector with Higgs portal

Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Physics, 2009.This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.Cataloged from student submitted PDF version of thesis.Includes bibliographical references (p. 67-75).In this thesis, we are investigating cosmological implications of hidden sector models which involve scalar fields that do not interact with the Standard Model gauge interactions, but couple directly to the Higgs field. We particularly focus on their relic particle density as a candidate for dark matter. For the case of hidden sector without a gauge field we have improved the accuracy of the bounds on the coupling constant and give bounds on the Lagrangian parameters. Models with Abelian and non-Abelian gauge fields are also studied with relic density bounds, BBN and galactic dynamics constraints. Several discussions on phase transitions and alternative dark matter candidates are included.by Serkan Cabi.Ph.D

Programmable Agents

We build deep RL agents that execute declarative programs expressed in formal language. The agents learn to ground the terms in this language in their environment, and can generalize their behavior at test time to execute new programs that refer to objects that were not referenced during training. The agents develop disentangled interpretable representations that allow them to generalize to a wide variety of zero-shot semantic tasks

Erratum: BRD7 regulates XBP1s' activity and glucose homeostasis through its interaction with the regulatory subunits of pi3k (Cell Metabolism (2014:20:73-84))

SummaryBromodomain-containing protein 7 (BRD7) is a member of the bromodomain-containing protein family that is known to play a role as tumor suppressors. Here, we show that BRD7 is a component of the unfolded protein response (UPR) signaling through its ability to regulate X-box binding protein 1 (XBP1) nuclear translocation. BRD7 interacts with the regulatory subunits of phosphatidylinositol 3-kinase (PI3K) and increases the nuclear translocation of both p85α and p85β and the spliced form of XBP1 (XBP1s). Deficiency of BRD7 blocks the nuclear translocation of XBP1s. Furthermore, our in vivo studies have shown that BRD7 protein levels are reduced in the liver of obese mice, and reinstating BRD7 levels in the liver restores XBP1s nuclear translocation, improves glucose homeostasis, and ultimately reduces the blood glucose levels in the obese and diabetic mouse models