16 research outputs found
Perturbation theory for optical excitations in the one-dimensional extended Peierls--Hubbard model
For the one-dimensional, extended Peierls--Hubbard model we calculate
analytically the ground-state energy and the single-particle gap to second
order in the Coulomb interaction for a given lattice dimerization. The
comparison with numerically exact data from the Density-Matrix Renormalization
Group shows that the ground-state energy is quantitatively reliable for Coulomb
parameters as large as the band width. The single-particle gap can almost
triple from its bare Peierls value before substantial deviations appear. For
the calculation of the dominant optical excitations, we follow two approaches.
In Wannier theory, we perturb the Wannier exciton states to second order. In
two-step perturbation theory, similar in spirit to the GW-BSE approach, we form
excitons from dressed electron-hole excitations. We find the Wannier approach
to be superior to the two-step perturbation theory. For singlet excitons,
Wannier theory is applicable up to Coulomb parameters as large as half band
width. For triplet excitons, second-order perturbation theory quickly fails
completely.Comment: 32 pages, 12 figures, submtted to JSTA
Excited States of Ladder-type Poly-p-phenylene Oligomers
Ground state properties and excited states of ladder-type paraphenylene
oligomers are calculated applying semiempirical methods for up to eleven
phenylene rings. The results are in qualitative agreement with experimental
data. A new scheme to interpret the excited states is developed which reveals
the excitonic nature of the excited states. The electron-hole pair of the
S1-state has a mean distance of approximately 4 Angstroem.Comment: 24 pages, 21 figure
Large-scale numerical investigations of the antiferromagnetic Heisenberg icosidodecahedron
We present up to date investigations of the antiferromagnetic Heisenberg
icosidodecahedron by means of the Density Matrix Renormalization Group method.
We compare our results with modern Correlator Product State as well as Lanczos
calculations.Comment: 20 pages, 11 figure
Uncertainties of ISO 3382-3 sound pressure level quantities
The ISO 3382-3 standard uses the measurable sound pressure based parameters D2,S and Lp,A,S,4 m to describe the acoustic properties of open-plan offices. As yet however, no treatment of the measurement uncertainty of these parameters according to the Guide to the expression of Uncertainty in Measurement (GUM) is to be found in the peer-reviewed literature. This technical note therefore describes how the measurement uncertainty can be declared according to GUM. The mathematical framework presented here can be used and expanded by other laboratories to derive their own uncertainty estimates. It is also applied in this document to 44 measurements yielding combined uncertainties for D2,S of 0.55 dB ≤ ≤ 0.67 dB and for Lp,A,S,4 m of 0.19 dB ≤ ≤ 0.83 dB. The implications of this result are discussed with regard to limit values in technical regulations
SMAD4 binds HOXA9 in the cytoplasm and protects primitive hematopoietic cells against nuclear activation by HOXA9 and leukemia transformation.
We studied leukemic stem cells (LSCs) in a Smad4(-/-) mouse model of acute myelogenous leukemia (AML) induced either by the HOXA9 gene or by the fusion oncogene NUP98-HOXA9. While HOXA9-SMAD4 complexes accumulate in the cytoplasm of normal hematopoietic stem- and progenitor cells (HSPCs) transduced with these oncogenes, there is no cytoplasmic accumulation of HOXA9 in Smad4(-/-) HSPCs and as a consequence increased levels of HOXA9 accumulate in the nucleus leading to increased immortalization in vitro. Loss of Smad4 accelerates the development of leukemia in vivo due to an increase in transformation of HSPCs. Therefore, the cytoplasmic binding of HOXA9 by SMAD4 is a mechanism to protect HOXA9-induced transformation of normal HSPCs. Since Smad4 is a potent tumor suppressor involved in growth control, we developed a strategy to modify the subcellular distribution of SMAD4. We successfully disrupted the interaction between HOXA9 and SMAD4 to activate the TGF-beta pathway and apoptosis, leading to a loss of LSCs. Together, these findings reveal a major role for Smad4 in the negative regulation of leukemia initiation and maintenance induced by HOXA9/NUP98-HOXA9 and provide strong evidence that antagonizing SMAD4 stabilization by these oncoproteins might be a promising novel therapeutic approach in leukemia
SMAD4 binds HOXA9 in the cytoplasm and protects primitive hematopoietic cells against nuclear activation by HOXA9 and leukemia transformation
We studied leukemic stem cells (LSCs) in a Smad4(-/-) mouse model of acute myelogenous leukemia (AML) induced either by the HOXA9 gene or by the fusion oncogene NUP98-HOXA9. While HOXA9-SMAD4 complexes accumulate in the cytoplasm of normal hematopoietic stem- and progenitor cells (HSPCs) transduced with these oncogenes, there is no cytoplasmic accumulation of HOXA9 in Smad4(-/-) HSPCs and as a consequence increased levels of HOXA9 accumulate in the nucleus leading to increased immortalization in vitro. Loss of Smad4 accelerates the development of leukemia in vivo due to an increase in transformation of HSPCs. Therefore, the cytoplasmic binding of HOXA9 by SMAD4 is a mechanism to protect HOXA9-induced transformation of normal HSPCs. Since Smad4 is a potent tumor suppressor involved in growth control, we developed a strategy to modify the subcellular distribution of SMAD4. We successfully disrupted the interaction between HOXA9 and SMAD4 to activate the TGF-beta pathway and apoptosis, leading to a loss of LSCs. Together, these findings reveal a major role for Smad4 in the negative regulation of leukemia initiation and maintenance induced by HOXA9/NUP98-HOXA9 and provide strong evidence that antagonizing SMAD4 stabilization by these oncoproteins might be a promising novel therapeutic approach in leukemia.status: publishe