467 research outputs found
Implications of Compressed Supersymmetry for Collider and Dark Matter Searches
Martin has proposed a scenario dubbed ``compressed supersymmetry'' (SUSY)
where the MSSM is the effective field theory between energy scales M_{\rm weak}
and M_{\rm GUT}, but with the GUT scale SU(3) gaugino mass M_3<< M_1 or M_2. As
a result, squark and gluino masses are suppressed relative to slepton, chargino
and neutralino masses, leading to a compressed sparticle mass spectrum, and
where the dark matter relic density in the early universe may be dominantly
governed by neutralino annihilation into ttbar pairs via exchange of a light
top squark. We explore the dark matter and collider signals expected from
compressed SUSY for two distinct model lines with differing assumptions about
GUT scale gaugino mass parameters. For dark matter signals, the compressed
squark spectrum leads to an enhancement in direct detection rates compared to
models with unified gaugino masses. Meanwhile, neutralino halo annihilation
rates to gamma rays and anti-matter are also enhanced relative to related
scenarios with unified gaugino masses but, depending on the halo dark matter
distribution, may yet be below the sensitivity of indirect searches underway.
In the case of collider signals, we compare the rates for the potentially
dominant decay modes of the stop_1 which may be expected to be produced in
cascade decay chains at the LHC: \tst_1\to c\tz_1 and \tst_1\to bW\tz_1. We
examine the extent to which multilepton signal rates are reduced when the
two-body decay mode dominates. For the model lines that we examine here, the
multi-lepton signals, though reduced, still remain observable at the LHC.Comment: 22 pages including 24 eps figure
A Super-Oxidized Radical Cationic Icosahedral Boron Cluster
While the icosahedral closo-[BāāHāā]Ā²ā» cluster does not display reversible electrochemical behavior, perfunctionalization of this species via substitution of all 12 BāH vertices with alkoxy or benzyloxy (OR) substituents engenders reversible redox chemistry, providing access to clusters in the dianionic, monoanionic, and neutral forms. Here, we evaluated the electrochemical behavior of the electron-rich Bāā(O-3-methylbutyl)āā (1) cluster and discovered that a new reversible redox event that gives rise to a fourth electronic state is accessible through one-electron oxidation of the neutral species. Chemical oxidation of 1 with [N(2,4-BrāCāHā)ā]Ā·āŗ afforded the isolable [1]Ā·āŗ cluster, which is the first example of an open-shell cationic Bāā cluster in which the unpaired electron is proposed to be delocalized throughout the boron cluster core. The oxidation of 1 is also chemically reversible, where treatment of [1]Ā·āŗ with ferrocene resulted in its reduction back to 1. The identity of [1]Ā·āŗ is supported by EPR, UVāvis, multinuclear NMR (Ā¹H, Ā¹Ā¹B), and X-ray photoelectron spectroscopic characterization
A Super-Oxidized Radical Cationic Icosahedral Boron Cluster
While the icosahedral closo-[BāāHāā]Ā²ā» cluster does not display reversible electrochemical behavior, perfunctionalization of this species via substitution of all 12 BāH vertices with alkoxy or benzyloxy (OR) substituents engenders reversible redox chemistry, providing access to clusters in the dianionic, monoanionic, and neutral forms. Here, we evaluated the electrochemical behavior of the electron-rich Bāā(O-3-methylbutyl)āā (1) cluster and discovered that a new reversible redox event that gives rise to a fourth electronic state is accessible through one-electron oxidation of the neutral species. Chemical oxidation of 1 with [N(2,4-BrāCāHā)ā]Ā·āŗ afforded the isolable [1]Ā·āŗ cluster, which is the first example of an open-shell cationic Bāā cluster in which the unpaired electron is proposed to be delocalized throughout the boron cluster core. The oxidation of 1 is also chemically reversible, where treatment of [1]Ā·āŗ with ferrocene resulted in its reduction back to 1. The identity of [1]Ā·āŗ is supported by EPR, UVāvis, multinuclear NMR (Ā¹H, Ā¹Ā¹B), and X-ray photoelectron spectroscopic characterization
Too Big to Fail ā U.S. Banksā Regulatory Alchemy: Converting an Obscure Agency Footnote into an āAt Willā Nullification of Dodd-Frankās Regulation of the Multi-Trillion Dollar Financial Swaps Market
The multi-trillion-dollar market for, what was at that time wholly unregulated, over-the-counter derivatives (āswapsā) is widely viewed as a principal cause of the 2008 worldwide financial meltdown. The Dodd-Frank Act, signed into law on July 21, 2010, was expressly considered by Congress to be a remedy for this troublesome deregulatory problem. The legislation required the swaps market to comply with a host of business conduct and anti-competitive protections, including that the swaps market be fully transparent to U.S. financial regulators, collateralized, and capitalized. The statute also expressly provides that it would cover foreign subsidiaries of big U.S. financial institutions if their swaps trading could adversely impact the U.S. economy or represent the use of extraterritorial trades as an attempt to āevadeā Dodd-Frank. In July 2013, the CFTC promulgated an 80-page, triple-columned, and single-spaced āguidanceā implementing Dodd-Frankās extraterritorial reach, i.e., that manner in which Dodd-Frank would apply to swaps transactions executed outside the United States. The key point of that guidance was that swaps trading within the āguaranteedā foreign subsidiaries of U.S. bank holding company swaps dealers were subject to all of Dodd-Frankās swaps regulations wherever in the world those subsidiariesā swaps were executed. At that time, the standardized industry swaps agreement contemplated that, inter alia, U.S. bank holding company swaps dealersā foreign subsidiaries would be āguaranteedā by their corporate parent, as was true since 1992. In August 2013, without notifying the CFTC, the principal U.S. bank holding company swaps dealer trade association privately circulated to its members standard contractual language that would, for the first time, ādeguaranteeā their foreign subsidiaries. By relying only on the obscure footnote 563 of the CFTC guidanceās 662 footnotes, the trade association assured its swaps dealer members that the newly deguaranteed foreign subsidiaries could (if they so chose) no longer be subject to Dodd-Frank. As a result, it has been reported (and it also has been understood by many experts within the swaps industry) that a substantial portion of the U.S. swaps market has shifted from the large U.S. bank holding companies swaps dealers and their U.S. affiliates to their newly deguaranteed āforeignā subsidiaries, with the attendant claim by these huge big U.S. bank swaps dealers that Dodd-Frank swaps regulation would not apply to these transactions. The CFTC also soon discovered that these huge U.S. bank holding company swaps dealers were āarranging, negotiating, and executingā (āANEā) these swaps in the United States with U.S. bank personnel and, only after execution in the U.S., were these swaps formally āassignedā to the U.S. banksā newly ādeguaranteedā foreign subsidiaries with the accompanying claim that these swaps, even though executed in the U.S., were not covered by Dodd-Frank. In October 2016, the CFTC proposed a rule that would have closed the ādeguaranteeā and āANEā loopholes completely. However, because it usually takes at least a year to finalize a āproposedā rule, this proposed rule closing the loopholes in question was not finalized prior to the inauguration of President Trump. All indications are that it will never be finalized during a Trump Administration. Thus, in the shadow of the recent tenth anniversary of the Lehman failure, there is an understanding among many market regulators and swaps trading experts that large portions of the swaps market have moved from U.S. bank holding company swaps dealers and their U.S. affiliates to their newly deguaranteed foreign affiliates where Dodd- Frank swaps regulation is not being followed. However, what has not moved abroad is the very real obligation of the lender of last resort to rescue these U.S. swaps dealer bank holding companies if they fail because of poorly regulated swaps in their deguaranteed foreign subsidiaries, i.e., the U.S. taxpayer. While relief is unlikely to be forthcoming from the Trump Administration or the Republican-controlled Senate, some other means will have to be found to avert another multi-trillion-dollar bank bailout and/or a financial calamity caused by poorly regulated swaps on the books of big U.S. banks. This paper notes that the relevant statutory framework affords state attorneys general and state financial regulators the right to bring so-called āparens patriaeā actions in federal district court to enforce, inter alia, Dodd- Frank on behalf of a stateās citizens. That kind of litigation to enforce the statuteās extraterritorial provisions is now badly needed
A p53-dependent mechanism underlies macrocytic anemia in a mouse model of human 5q- syndrome.
The identification of the genes associated with chromosomal translocation breakpoints has fundamentally changed understanding of the molecular basis of hematological malignancies. By contrast, the study of chromosomal deletions has been hampered by the large number of genes deleted and the complexity of their analysis. We report the generation of a mouse model for human 5q- syndrome using large-scale chromosomal engineering. Haploinsufficiency of the Cd74-Nid67 interval (containing Rps14, encoding the ribosomal protein S14) caused macrocytic anemia, prominent erythroid dysplasia and monolobulated megakaryocytes in the bone marrow. These effects were associated with defective bone marrow progenitor development, the appearance of bone marrow cells expressing high amounts of the tumor suppressor p53 and increased bone marrow cell apoptosis. Notably, intercrossing with p53-deficient mice completely rescued the progenitor cell defect, restoring common myeloid progenitor and megakaryocytic-erythroid progenitor, granulocyte-monocyte progenitor and hematopoietic stem cell bone marrow populations. This mouse model suggests that a p53-dependent mechanism underlies the pathophysiology of the 5q- syndrome
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