Diffusion of fluorine adatoms on doped graphene

We calculate the diffusion barrier of fluorine adatoms on doped graphene in the diluted limit using Density Functional Theory. We found that the barrier $\Delta$ strongly depends on the magnitude and character of the graphene's doping ($\delta n$): it increases for hole doping ($\delta n<0$) and decreases for electron doping ($\delta n>0$). Near the neutrality point the functional dependence can be approximately by $\Delta=\Delta_0-\alpha\, \delta n$ where $\alpha\simeq6\times10^{-12}$ meVcm$^2$. This effect leads to significant changes of the diffusion constant with doping even at room temperature and could also affect the low temperature diffusion dynamics due to the presence of substrate induced charge puddles. In addition, this might open up the possibility to engineer the F dynamics on graphene by using local gates.Comment: 4 pages, 4 figure

L\'evy flights due to anisotropic disorder in graphene

We study transport properties of graphene with anisotropically distributed on-site impurities (adatoms) that are randomly placed on every third line drawn along carbon bonds. We show that stripe states characterized by strongly suppressed back-scattering are formed in this model in the direction of the lines. The system reveals L\'evy-flight transport in stripe direction such that the corresponding conductivity increases as the square root of the system length. Thus, adding this type of disorder to clean graphene near the Dirac point strongly enhances the conductivity, which is in stark contrast with a fully random distribution of on-site impurities which leads to Anderson localization. The effect is demonstrated both by numerical simulations using the Kwant code and by an analytical theory based on the self-consistent $T$-matrix approximation.Comment: 11 pages, 6 figure

Quantum Hall criticality and localization in graphene with short-range impurities at the Dirac point

We explore the longitudinal conductivity of graphene at the Dirac point in a strong magnetic field with two types of short-range scatterers: adatoms that mix the valleys and "scalar" impurities that do not mix them. A scattering theory for the Dirac equation is employed to express the conductance of a graphene sample as a function of impurity coordinates; an averaging over impurity positions is then performed numerically. The conductivity $\sigma$ is equal to the ballistic value $4e^2/\pi h$ for each disorder realization provided the number of flux quanta considerably exceeds the number of impurities. For weaker fields, the conductivity in the presence of scalar impurities scales to the quantum-Hall critical point with $\sigma \simeq 4 \times 0.4 e^2/h$ at half filling or to zero away from half filling due to the onset of Anderson localization. For adatoms, the localization behavior is obtained also at half filling due to splitting of the critical energy by intervalley scattering. Our results reveal a complex scaling flow governed by fixed points of different symmetry classes: remarkably, all key manifestations of Anderson localization and criticality in two dimensions are observed numerically in a single setup.Comment: 17 pages, 4 figure

The polo-like kinase 1 (PLK1) inhibitor NMS-P937 is effective in a new model of disseminated primary CD56+ acute monoblastic leukaemia

CD56 is expressed in 15–20% of acute myeloid leukaemias (AML) and is associated with extramedullary diffusion, multidrug resistance and poor prognosis. We describe the establishment and characterisation of a novel disseminated model of AML (AML-NS8), generated by injection into mice of leukaemic blasts freshly isolated from a patient with an aggressive CD56+ monoblastic AML (M5a). The model reproduced typical manifestations of this leukaemia, including presence of extramedullary masses and central nervous system involvement, and the original phenotype, karyotype and genotype of leukaemic cells were retained in vivo. Recently Polo-Like Kinase 1 (PLK1) has emerged as a new candidate drug target in AML. We therefore tested our PLK1 inhibitor NMS-P937 in this model either in the engraftment or in the established disease settings. Both schedules showed good efficacy compared to standard therapies, with a significant increase in median survival time (MST) expecially in the established disease setting (MST = 28, 36, 62 days for vehicle, cytarabine and NMS-P937, respectively). Importantly, we could also demonstrate that NMS-P937 induced specific biomarker modulation in extramedullary tissues. This new in vivo model of CD56+ AML that recapitulates the human tumour lends support for the therapeutic use of PLK1 inhibitors in AML

Umweltbildungsinitiative 'Biodiversitaet und Umweltbildung in Seenregionen'. Bd. 1, 2 und 3 Abschlussbericht

Published in 3 volumesSIGLEAvailable from TIB Hannover: F02B480: F02B481: F02B482 / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekDeutsche Bundesstiftung Umwelt, Osnabrueck (Germany)DEGerman

Novel RUNX1 isoforms determine the fate of acute myeloid leukemia cells by controlling CD56 expression.

CD56(high) acute myeloid leukemias (AMLs) have a poor prognosis, but it has been unclear how CD56 expression is controlled and how it relates to clinical aggressiveness. We show that CD56 expression on AML cells correlates with an abnormal expression pattern of runt-related transcription factor 1 (RUNX1) isoforms. Whereas full-length p48 RUNX1 (p48) up-regulated CD56 in AML cells, 3 previously unknown shorter RUNX1 isoforms, p38a, p30, and p24, suppressed CD56 expression. Both p48 and CD56 induced nuclear translocation of nuclear factor (NF)-kappaB and increased bcl2L12 expression, and inhibition of this pathway by small inhibitory RNA-mediated p48 knock down or NF-kappaB blockade substantially increased apoptosis in CD56(+) AML cell lines. These findings indicate the potential for new therapy of CD56(high) AML by suppression of the "overactive" RUNX1/CD56/NF-kappaB signaling pathway(s)