11,408 research outputs found
Understanding the internal structures of the , , and
We investigate the newly observed and based on the
diquark-antidiquark configuration within the framework of QCD sum rules. Both
of them may be interpreted as the -wave tetraquark states
of , but with opposite color structures, which is remarkably similar
to the result obtained in Ref.~\cite{Chen:2010ze} that the and
can be both interpreted as the -wave tetraquark
states of , also with opposite color structures. However, the
extracted masses and these suggested assignments to these states do depend
on these running quark masses where m_s (2 \mbox{ GeV}) = 95 \pm 5 MeV and
GeV. As a byproduct, the masses of the
hidden-bottom partner states of the and are extracted to be
both around 10.64 GeV, which can be searched for in the
invariant mass distribution.Comment: 6 pages, 4 figures. Accepted by Eur. Phys. J.
resonance as a tetraquark state and its isospin partner
We systematically construct tetraquark currents of and
classify them into types (antisymmetric), (symmetric)
and (mixed), based on flavor symmetries of diquarks and
antidiquarks composing the tetra quark currents. We use tetraquark currents of
type to perform QCD sum rule analyses, and find a tetraquark
current with quark contents ( or )
leading to a mass of GeV consistent with the state
recently observed by the COMPASS collaboration. Our results support tetraquark
explanations for both and , assuming that they are
isospin partners. We also study their possible decay patterns. As tetraquark
candidates, the possible decay modes of are -wave and -wave while
the possible decay patterns of are -wave and -wave . We speculate that
is partly responsible for the large isospin violation in the
decay mode which is reported by BESIII
collaboration in the process.Comment: 15 pages, 8 figures. Accepted by Phys. Rev.
Overexpression of an isoform of AML1 in acute leukemia and its potential role in leukemogenesis
AML1/RUNX1 is a critical transcription factor in hematopoietic cell differentiation and proliferation. From the _AML1_ gene, at least three isoforms, _AML1a_, _AML1b_ and _AML1c_, are produced through alternative splicing. AML1a interferes with the function of AML1b/1c, which are often called AML1. In the current study, we found a higher expression level of _AML1a_ in ALL patients in comparison to the controls. Additionally, AML1a represses transcription from promotor of macrophage-colony simulating factor receptor (M-CSFR) mediated by AML1b, indicating that AML1a antagonized the effect of AML1b. In order to investigate the role of _AML1a_ in hematopoiesis and leukemogenesis _in vivo_, bone marrow mononuclear cells (BMMNCs) from mice were transduced with AML1a and transplanted into lethally irradiated mice, which develop lymphoblastic leukemia after transplantation. Taken together, these results indicate that overexpression of AML1a may be an important contributing factor to leukemogenesis
- …