478 research outputs found
Photodetection of propagating quantum microwaves in circuit QED
We develop the theory of a metamaterial composed of an array of discrete
quantum absorbers inside a one-dimensional waveguide that implements a
high-efficiency microwave photon detector. A basic design consists of a few
metastable superconducting nanocircuits spread inside and coupled to a
one-dimensional waveguide in a circuit QED setup. The arrival of a {\it
propagating} quantum microwave field induces an irreversible change in the
population of the internal levels of the absorbers, due to a selective
absorption of photon excitations. This design is studied using a formal but
simple quantum field theory, which allows us to evaluate the single-photon
absorption efficiency for one and many absorber setups. As an example, we
consider a particular design that combines a coplanar coaxial waveguide with
superconducting phase qubits, a natural but not exclusive playground for
experimental implementations. This work and a possible experimental realization
may stimulate the possible arrival of "all-optical" quantum information
processing with propagating quantum microwaves, where a microwave photodetector
could play a key role.Comment: 27 pages, submitted to Physica Scripta for Nobel Symposium on "Qubits
for Quantum Information", 200
Collisional kinetics of non-uniform electric field, low-pressure, direct-current discharges in H
A model of the collisional kinetics of energetic hydrogen atoms, molecules,
and ions in pure H discharges is used to predict H emission
profiles and spatial distributions of emission from the cathode regions of
low-pressure, weakly-ionized discharges for comparison with a wide variety of
experiments. Positive and negative ion energy distributions are also predicted.
The model developed for spatially uniform electric fields and current densities
less than A/m is extended to non-uniform electric fields, current
densities of A/m, and electric field to gas density ratios MTd at 0.002 to 5 Torr pressure. (1 Td = V m and 1 Torr =
133 Pa) The observed far-wing Doppler broadening and spatial distribution of
the H emission is consistent with reactions among H, H,
H, and H ions, fast H atoms, and fast H molecules, and with
reflection, excitation, and attachment to fast H atoms at surfaces. The
H excitation and H formation occur principally by collisions of
fast H, fast H, and H with H. Simplifications include using a
one-dimensional geometry, a multi-beam transport model, and the average
cathode-fall electric field. The H emission is linear with current
density over eight orders of magnitude. The calculated ion energy distributions
agree satisfactorily with experiment for H and H, but are only in
qualitative agreement for H and H. The experiments successfully modeled
range from short-gap, parallel-plane glow discharges to beam-like,
electrostatic-confinement discharges.Comment: Submitted to Plasmas Sources Science and Technology 8/18/201
Limitations of Gene Duplication Models: Evolution of Modules in Protein Interaction Networks
It has been generally acknowledged that the module structure of protein interaction networks plays a crucial role with respect to the functional understanding of these networks. In this paper, we study evolutionary aspects of the module structure of protein interaction networks, which forms a mesoscopic level of description with respect to the architectural principles of networks. The purpose of this paper is to investigate limitations of well known gene duplication models by showing that these models are lacking crucial structural features present in protein interaction networks on a mesoscopic scale. This observation reveals our incomplete understanding of the structural evolution of protein networks on the module level
Nodal dynamics, not degree distributions, determine the structural controllability of complex networks
Structural controllability has been proposed as an analytical framework for
making predictions regarding the control of complex networks across myriad
disciplines in the physical and life sciences (Liu et al.,
Nature:473(7346):167-173, 2011). Although the integration of control theory and
network analysis is important, we argue that the application of the structural
controllability framework to most if not all real-world networks leads to the
conclusion that a single control input, applied to the power dominating set
(PDS), is all that is needed for structural controllability. This result is
consistent with the well-known fact that controllability and its dual
observability are generic properties of systems. We argue that more important
than issues of structural controllability are the questions of whether a system
is almost uncontrollable, whether it is almost unobservable, and whether it
possesses almost pole-zero cancellations.Comment: 1 Figures, 6 page
Inferring the conservative causal core of gene regulatory networks
<p>Abstract</p> <p>Background</p> <p>Inferring gene regulatory networks from large-scale expression data is an important problem that received much attention in recent years. These networks have the potential to gain insights into causal molecular interactions of biological processes. Hence, from a methodological point of view, reliable estimation methods based on observational data are needed to approach this problem practically.</p> <p>Results</p> <p>In this paper, we introduce a novel gene regulatory network inference (GRNI) algorithm, called C3NET. We compare C3NET with four well known methods, ARACNE, CLR, MRNET and RN, conducting in-depth numerical ensemble simulations and demonstrate also for biological expression data from <it>E. coli </it>that C3NET performs consistently better than the best known GRNI methods in the literature. In addition, it has also a low computational complexity. Since C3NET is based on estimates of mutual information values in conjunction with a maximization step, our numerical investigations demonstrate that our inference algorithm exploits causal structural information in the data efficiently.</p> <p>Conclusions</p> <p>For systems biology to succeed in the long run, it is of crucial importance to establish methods that extract large-scale gene networks from high-throughput data that reflect the underlying causal interactions among genes or gene products. Our method can contribute to this endeavor by demonstrating that an inference algorithm with a neat design permits not only a more intuitive and possibly biological interpretation of its working mechanism but can also result in superior results.</p
An approach for the identification of targets specific to bone metastasis using cancer genes interactome and gene ontology analysis
Metastasis is one of the most enigmatic aspects of cancer pathogenesis and is
a major cause of cancer-associated mortality. Secondary bone cancer (SBC) is a
complex disease caused by metastasis of tumor cells from their primary site and
is characterized by intricate interplay of molecular interactions.
Identification of targets for multifactorial diseases such as SBC, the most
frequent complication of breast and prostate cancers, is a challenge. Towards
achieving our aim of identification of targets specific to SBC, we constructed
a 'Cancer Genes Network', a representative protein interactome of cancer genes.
Using graph theoretical methods, we obtained a set of key genes that are
relevant for generic mechanisms of cancers and have a role in biological
essentiality. We also compiled a curated dataset of 391 SBC genes from
published literature which serves as a basis of ontological correlates of
secondary bone cancer. Building on these results, we implement a strategy based
on generic cancer genes, SBC genes and gene ontology enrichment method, to
obtain a set of targets that are specific to bone metastasis. Through this
study, we present an approach for probing one of the major complications in
cancers, namely, metastasis. The results on genes that play generic roles in
cancer phenotype, obtained by network analysis of 'Cancer Genes Network', have
broader implications in understanding the role of molecular regulators in
mechanisms of cancers. Specifically, our study provides a set of potential
targets that are of ontological and regulatory relevance to secondary bone
cancer.Comment: 54 pages (19 pages main text; 11 Figures; 26 pages of supplementary
information). Revised after critical reviews. Accepted for Publication in
PLoS ON
Functional assays to determine the significance of two common XPC 3'UTR variants found in bladder cancer patients
<p>Abstract</p> <p>Background</p> <p><it>XPC </it>is involved in the nucleotide excision repair of DNA damaged by carcinogens known to cause bladder cancer. Individuals homozygous for the variant allele of <it>XPC </it>c.1496C > T (p.Ala499Val) were shown in a large pooled analysis to have an increased bladder cancer risk, and we found two 3'UTR variants, *611T > A and c.*618A > G, to be in strong linkage disequilibrium with c.1496T. Here we determined if these two 3'UTR variants can affect mRNA stability and assessed the impact of all three variants on mRNA and protein expression.</p> <p>Methods</p> <p><it>In vitro </it>mRNA stability assays were performed and mRNA and protein expression measured both in plasmid-based assays and in lymphocytes and lymphoblastoid cell lines from bladder and breast cancer patients.</p> <p>Results</p> <p>The two 3'UTR variants were associated with reduced protein and mRNA expression in plasmid-based assays, suggesting an effect on mRNA stability and/or transcription/translation. A near-significant reduction in XPC protein expression (p = 0.058) was detected in lymphoblastoid cell lines homozygous for these alleles but no differences in mRNA stability in these lines was found or in mRNA or protein levels in lymphocytes heterozygous for these alleles.</p> <p>Conclusion</p> <p>The two 3'UTR variants may be the variants underlying the association of c.1496C > T and bladder cancer risk acting via a mechanism modulating protein expression.</p
Inferring the conservative causal core of gene regulatory networks
<p>Abstract</p> <p>Background</p> <p>Inferring gene regulatory networks from large-scale expression data is an important problem that received much attention in recent years. These networks have the potential to gain insights into causal molecular interactions of biological processes. Hence, from a methodological point of view, reliable estimation methods based on observational data are needed to approach this problem practically.</p> <p>Results</p> <p>In this paper, we introduce a novel gene regulatory network inference (GRNI) algorithm, called C3NET. We compare C3NET with four well known methods, ARACNE, CLR, MRNET and RN, conducting in-depth numerical ensemble simulations and demonstrate also for biological expression data from <it>E. coli </it>that C3NET performs consistently better than the best known GRNI methods in the literature. In addition, it has also a low computational complexity. Since C3NET is based on estimates of mutual information values in conjunction with a maximization step, our numerical investigations demonstrate that our inference algorithm exploits causal structural information in the data efficiently.</p> <p>Conclusions</p> <p>For systems biology to succeed in the long run, it is of crucial importance to establish methods that extract large-scale gene networks from high-throughput data that reflect the underlying causal interactions among genes or gene products. Our method can contribute to this endeavor by demonstrating that an inference algorithm with a neat design permits not only a more intuitive and possibly biological interpretation of its working mechanism but can also result in superior results.</p
Compartmental Genomics in Living Cells Revealed by Single-Cell Nanobiopsy
The ability to study the molecular biology of living single cells in heterogeneous cell populations is essential for next generation analysis of cellular circuitry and function. Here, we developed a single-cell nanobiopsy platform based on scanning ion conductance microscopy (SICM) for continuous sampling of intracellular content from individual cells. The nanobiopsy platform uses electrowetting within a nanopipette to extract cellular material from living cells with minimal disruption of the cellular milieu. We demonstrate the subcellular resolution of the nanobiopsy platform by isolating small subpopulations of mitochondria from single living cells, and quantify mutant mitochondrial genomes in those single cells with high throughput sequencing technology. These findings may provide the foundation for dynamic subcellular genomic analysis
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