29 research outputs found
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
strongly depends on the magnitude and character of the graphene's
doping (): it increases for hole doping () and decreases
for electron doping (). Near the neutrality point the functional
dependence can be approximately by where
meVcm. 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
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 is
equal to the ballistic value 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 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
Small extracellular vesicle-derived miR-574-5p regulates PGE2-biosynthesis via TLR7/8 in lung cancer
Intercellular communication plays an essential role in lung cancer (LC). One of the major players in cell-cell-communication is small extracellular vesicles (sEV). SEV trigger various biological responses by transporting cellular cargo to target cells. One essential sEV component are microRNAs (miRs), whose transport has recently attracted increasing research interest. We report that prostaglandin E-2 (PGE(2)), a key inflammatory lipid mediator, specifically induces the sorting of miR-574-5p in sEV of A549 and 2106T cells. We found that sEV-derived miR-574-5p activates Toll-like receptors (TLR) 7/8, thereby decreasing PGE(2)-levels. In contrast, intracellular miR-574-5p induces PGE(2)-biosynthesis. Consequently, the combination of intracellular and sEV-derived miR-574-5p controls PGE(2)-levels via a feedback loop. This was only observed in adeno- but not in squamous cell carcinoma, indicating a cell-specific response to sEV-derived miRs, which might be due to unique tetraspanin compositions. Hence, we describe a novel function of miR-574-5p unique to adenocarcinoma. Intracellular miR-574-5p induces PGE(2) and thus the secretion of sEV-derived miR-574-5p, which in turn decreases PGE(2)-biosynthesis in recipient cells