Weak-triplet, color-octet scalars and the CDF dijet excess

We extend the standard model to include a weak-triplet and color-octet scalar. This `octo-triplet' field consists of three particles, two charged and one neutral, whose masses and renormalizable interactions depend only on two new parameters. The charged octo-triplet decay into a W boson and a gluon is suppressed by a loop factor and an accidental cancellation. Thus, the main decays of the charged octo-triplet may occur through higher-dimensional operators, mediated by a heavy vectorlike fermion, into quark pairs. For an octo-triplet mass below the t\bar{b} threshold, the decay into Wb\bar{b} or Wb\bar{s} through an off-shell top quark has a width comparable to that into c\bar{s} or c\bar{b}. Pair production with one octo-triplet decaying into two jets and the other decaying into a W and two soft b jets may explain the dijet-plus-W excess reported by the CDF Collaboration. Using a few kinematic distributions, we compare two mechanisms of octo-triplet pair production: through an s-channel coloron and through the coupling to gluons. The higher-dimensional operators that allow dijet decays also lead to CP violation in B_s - \bar B_s mixing.Comment: 18 pages. New CDF kinematic distributions using 7.3 fb^{-1} compared to both resonant and gluon-induced pair production of octets. Corrections in Section 3.1. Comment on the D0 Wjj result included in Section 3.3. Implications for LHC expanded in Section 3.

Light Weakly Coupled Axial Forces: Models, Constraints, and Projections

We investigate the landscape of constraints on MeV-GeV scale, hidden U(1) forces with nonzero axial-vector couplings to Standard Model fermions. While the purely vector-coupled dark photon, which may arise from kinetic mixing, is a well-motivated scenario, several MeV-scale anomalies motivate a theory with axial couplings which can be UV-completed consistent with Standard Model gauge invariance. Moreover, existing constraints on dark photons depend on products of various combinations of axial and vector couplings, making it difficult to isolate the effects of axial couplings for particular flavors of SM fermions. We present a representative renormalizable, UV-complete model of a dark photon with adjustable axial and vector couplings, discuss its general features, and show how some UV constraints may be relaxed in a model with nonrenormalizable Yukawa couplings at the expense of fine-tuning. We survey the existing parameter space and the projected reach of planned experiments, briefly commenting on the relevance of the allowed parameter space to low-energy anomalies in pi^0 and 8-Be* decay.Comment: 30 pages, 5 figures, 4 tables. v2: format changed to JHEP, typos fixed, references adde

HIF and c-Myc: Sibling Rivals for Control of Cancer Cell Metabolism and Proliferation

O2 deprivation (hypoxia) and cellular proliferation engage opposite cellular pathways, yet often coexist during tumor growth. The ability of cells to grow during hypoxia results in part from crosstalk between hypoxia-inducible factors (HIFs) and the proto-oncogene c-Myc. Acting alone, HIF and c-Myc partially regulate complex adaptations undertaken by tumor cells growing in low O2. However, acting in concert these transcription factors reprogram metabolism, protein synthesis, and cell cycle progression, to “fine tune” adaptive responses to hypoxic environments

Real-Time Hemodynamic Evidence Supporting the Safety of Acute Isometric Exercise

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Symmetric Jacobians

This article is about polynomial maps with a certain symmetry and/or antisymmetry in their Jacobians, and whether the Jacobian Conjecture is satisfied for such maps, or whether it is sufficient to prove the Jacobian Conjecture for such maps. For instance, we show that it suffices to prove the Jacobian conjecture for polynomial maps x + H over C such that JH satisfies all symmetries of the square, where H is homogeneous of arbitrary degree d >= 3.Comment: 18 pages, minor corrections, grayscale eepic boxes have been replaced by colorful tikz boxe

A single H/ACA small nucleolar RNA mediates tumor suppression downstream of oncogenic RAS.

Small nucleolar RNAs (snoRNAs) are a diverse group of non-coding RNAs that direct chemical modifications at specific residues on other RNA molecules, primarily on ribosomal RNA (rRNA). SnoRNAs are altered in several cancers; however, their role in cell homeostasis as well as in cellular transformation remains poorly explored. Here, we show that specific subsets of snoRNAs are differentially regulated during the earliest cellular response to oncogenic RASG12V expression. We describe a novel function for one H/ACA snoRNA, SNORA24, which guides two pseudouridine modifications within the small ribosomal subunit, in RAS-induced senescence in vivo. We find that in mouse models, loss of Snora24 cooperates with RASG12V to promote the development of liver cancer that closely resembles human steatohepatitic hepatocellular carcinoma (HCC). From a clinical perspective, we further show that human HCCs with low SNORA24 expression display increased lipid content and are associated with poor patient survival. We next asked whether ribosomes lacking SNORA24-guided pseudouridine modifications on 18S rRNA have alterations in their biophysical properties. Single-molecule Fluorescence Resonance Energy Transfer (FRET) analyses revealed that these ribosomes exhibit perturbations in aminoacyl-transfer RNA (aa-tRNA) selection and altered pre-translocation ribosome complex dynamics. Furthermore, we find that HCC cells lacking SNORA24-guided pseudouridine modifications have increased translational miscoding and stop codon readthrough frequencies. These findings highlight a role for specific snoRNAs in safeguarding against oncogenic insult and demonstrate a functional link between H/ACA snoRNAs regulated by RAS and the biophysical properties of ribosomes in cancer