180 research outputs found
Barrier-controlled carrier transport in microcrystalline semiconducting materials: Description within a unified model
A recently developed model that unifies the ballistic and diffusive transport
mechanisms is applied in a theoretical study of carrier transport across
potential barriers at grain boundaries in microcrystalline semiconducting
materials. In the unified model, the conductance depends on the detailed
structure of the band edge profile and in a nonlinear way on the carrier mean
free path. Equilibrium band edge profiles are calculated within the trapping
model for samples made up of a linear chain of identical grains. Quantum
corrections allowing for tunneling are included in the calculation of electron
mobilities. The dependence of the mobilities on carrier mean free path, grain
length, number of grains, and temperature is examined, and appreciable
departures from the results of the thermionic-field-emission model are found.
Specifically, the unified model is applied in an analysis of Hall mobility data
for n-type microcrystalline Si thin films in the range of thermally activated
transport. Owing mainly to the effect of tunneling, potential barrier heights
derived from the data are substantially larger than the activation energies of
the Hall mobilities. The specific features of the unified model, however,
cannot be resolved within the rather large uncertainties of the analysis.Comment: REVTex, 19 pages, 9 figures; to appear in J. Appl. Phy
Combined population dynamics and entropy modelling supports patient stratification in chronic myeloid leukemia
Modelling the parameters of multistep carcinogenesis is key for a better understanding of cancer
progression, biomarker identification and the design of individualized therapies. Using chronic
myeloid leukemia (CML) as a paradigm for hierarchical disease evolution we show that combined
population dynamic modelling and CML patient biopsy genomic analysis enables patient stratification
at unprecedented resolution. Linking CD34+ similarity as a disease progression marker to patientderived
gene expression entropy separated established CML progression stages and uncovered
additional heterogeneity within disease stages. Importantly, our patient data informed model enables
quantitative approximation of individual patientsâ disease history within chronic phase (CP) and
significantly separates âearlyâ from âlateâ CP. Our findings provide a novel rationale for personalized
and genome-informed disease progression risk assessment that is independent and complementary to
conventional measures of CML disease burden and prognosis
Unsuitability of the moving light clock system for the Lorentz factor derivation
The moving light clock system was analyzed with respect to the orientation of
the wavefront of the light pulse observed in the moving and stationary frames
of reference. The plane wavefront of the light pulse was oriented horizontally
in both the frames. The wavefront observed in the stationary frame was not
perpendicular to the direction of the light pulse propagation. This showed
different characteristics of the light pulse than that assumed in the Lorentz
factor derivation. According to the horizontal orientation of the wavefront,
velocity c was determined as the vertical component of the light pulse motion
observed in the stationary frame. Application of this velocity distribution in
the Lorentz factor derivation showed the same travel time for the light pulse
observed in the moving and stationary frames of reference. The moving light
clock system was therefore found to be unsuitable for the Lorentz factor
derivation and illustration of time dilation, and shown to illustrate the
relativity of the observation of light rather than the relativity of time.Comment: 4 pages, 5 figure
Mapping interactions with the chaperone network reveals factors that protect against tau aggregation.
A network of molecular chaperones is known to bind proteins ('clients') and balance their folding, function and turnover. However, it is often unclear which chaperones are critical for selective recognition of individual clients. It is also not clear why these key chaperones might fail in protein-aggregation diseases. Here, we utilized human microtubule-associated protein tau (MAPT or tau) as a model client to survey interactions between ~30 purified chaperones and ~20 disease-associated tau variants (~600 combinations). From this large-scale analysis, we identified human DnaJA2 as an unexpected, but potent, inhibitor of tau aggregation. DnaJA2 levels were correlated with tau pathology in human brains, supporting the idea that it is an important regulator of tau homeostasis. Of note, we found that some disease-associated tau variants were relatively immune to interactions with chaperones, suggesting a model in which avoiding physical recognition by chaperone networks may contribute to disease
Quantization of the interior Schwarzschild black hole
We study a Hamiltonian quantum formalism of a spherically symmetric
space-time which can be identified with the interior of a Schwarzschild black
hole. The phase space of this model is spanned by two dynamical variables and
their conjugate momenta. It is shown that the classical Lagrangian of the model
gives rise the interior metric of a Schwarzschild black hole. We also show that
the the mass of such a system is a Dirac observable and then by quantization of
the model by Wheeler-DeWitt approach and constructing suitable wave packets we
get the mass spectrum of the black hole.Comment: 12 pages, 1 figure, revised versio
A Computational Approach to Analyze the Mechanism of Action of the Kinase Inhibitor Bafetinib
Prediction of drug action in human cells is a major challenge in biomedical research. Additionally, there is strong interest in finding new applications for approved drugs and identifying potential side effects. We present a computational strategy to predict mechanisms, risks and potential new domains of drug treatment on the basis of target profiles acquired through chemical proteomics. Functional protein-protein interaction networks that share one biological function are constructed and their crosstalk with the drug is scored regarding function disruption. We apply this procedure to the target profile of the second-generation BCR-ABL inhibitor bafetinib which is in development for the treatment of imatinib-resistant chronic myeloid leukemia. Beside the well known effect on apoptosis, we propose potential treatment of lung cancer and IGF1R expressing blast crisis
PPR proteins - orchestrators of organelle RNA metabolism.
Pentatricopeptide repeat (PPR) proteins are important RNA regulators in chloroplasts and mitochondria, aiding in RNA editing, maturation, stabilisation or intron splicing, and in transcription and translation of organellar genes. In this review, we summarise all PPR proteins documented so far in plants and the green alga Chlamydomonas. By further analysis of the known target RNAs from Arabidopsis thaliana PPR proteins, we find that all organellar-encoded complexes are regulated by these proteins, although to differing extents. In particular, the orthologous complexes of NADH dehydrogenase (Complex I) in the mitochondria and NADH dehydrogenase-like (NDH) complex in the chloroplast were the most regulated, with respectively 60 and 28% of all characterised A. thaliana PPR proteins targeting their genes
The disruption of proteostasis in neurodegenerative diseases
Cells count on surveillance systems to monitor and protect the cellular proteome which, besides being highly heterogeneous, is constantly being challenged by intrinsic and environmental factors. In this context, the proteostasis network (PN) is essential to achieve a stable and functional proteome. Disruption of the PN is associated with aging and can lead to and/or potentiate the occurrence of many neurodegenerative diseases (ND). This not only emphasizes the importance of the PN in health span and aging but also how its modulation can be a potential target for intervention and treatment of human diseases.info:eu-repo/semantics/publishedVersio
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