45 research outputs found
Random Convex Hulls and Extreme Value Statistics
In this paper we study the statistical properties of convex hulls of
random points in a plane chosen according to a given distribution. The points
may be chosen independently or they may be correlated. After a non-exhaustive
survey of the somewhat sporadic literature and diverse methods used in the
random convex hull problem, we present a unifying approach, based on the notion
of support function of a closed curve and the associated Cauchy's formulae,
that allows us to compute exactly the mean perimeter and the mean area enclosed
by the convex polygon both in case of independent as well as correlated points.
Our method demonstrates a beautiful link between the random convex hull problem
and the subject of extreme value statistics. As an example of correlated
points, we study here in detail the case when the points represent the vertices
of independent random walks. In the continuum time limit this reduces to
independent planar Brownian trajectories for which we compute exactly, for
all , the mean perimeter and the mean area of their global convex hull. Our
results have relevant applications in ecology in estimating the home range of a
herd of animals. Some of these results were announced recently in a short
communication [Phys. Rev. Lett. {\bf 103}, 140602 (2009)].Comment: 61 pages (pedagogical review); invited contribution to the special
issue of J. Stat. Phys. celebrating the 50 years of Yeshiba/Rutgers meeting
Expression Analysis of the Theileria parva Subtelomere-Encoded Variable Secreted Protein Gene Family
Background
The intracellular protozoan parasite Theileria parva transforms bovine lymphocytes inducing uncontrolled proliferation. Proteins released from the parasite are assumed to contribute to phenotypic changes of the host cell and parasite persistence. With 85 members, genes encoding subtelomeric variable secreted proteins (SVSPs) form the largest gene family in T. parva. The majority of SVSPs contain predicted signal peptides, suggesting secretion into the host cell cytoplasm.
Methodology/Principal Findings
We analysed SVSP expression in T. parva-transformed cell lines established in vitro by infection of T or B lymphocytes with cloned T. parva parasites. Microarray and quantitative real-time PCR analysis revealed mRNA expression for a wide range of SVSP genes. The pattern of mRNA expression was largely defined by the parasite genotype and not by host background or cell type, and found to be relatively stable in vitro over a period of two months. Interestingly, immunofluorescence analysis carried out on cell lines established from a cloned parasite showed that expression of a single SVSP encoded by TP03_0882 is limited to only a small percentage of parasites. Epitope-tagged TP03_0882 expressed in mammalian cells was found to translocate into the nucleus, a process that could be attributed to two different nuclear localisation signals.
Conclusions
Our analysis reveals a complex pattern of Theileria SVSP mRNA expression, which depends on the parasite genotype. Whereas in cell lines established from a cloned parasite transcripts can be found corresponding to a wide range of SVSP genes, only a minority of parasites appear to express a particular SVSP protein. The fact that a number of SVSPs contain functional nuclear localisation signals suggests that proteins released from the parasite could contribute to phenotypic changes of the host cell. This initial characterisation will facilitate future studies on the regulation of SVSP gene expression and the potential biological role of these enigmatic proteins
Qualitative-feed-restricted heavy swine: meat quality and morpho-histochemical characteristics of muscle fibers
Enhanced Conformational Sampling using Replica Exchange with Collective-Variable Tempering
The computational study of conformational transitions in RNA and proteins with atomistic molecular dynamics often requires suitable enhanced sampling techniques. We here introduce a novel method where concurrent metadynamics are integrated in a Hamiltonian replica-exchange scheme. The ladder of replicas is built with different strength of the bias potential exploiting the tunability of well-tempered metadynamics. Using this method, free-energy barriers of individual collective variables are significantly reduced compared with simple force-field scaling. The introduced methodology is flexible and allows adaptive bias potentials to be self-consistently constructed for a large number of simple collective variables, such as distances and dihedral angles. The method is tested on alanine dipeptide and applied to the difficult problem of conformational sampling in a tetranucleotide
Counting the Faces of Randomly-Projected Hypercubes and Orthants, with Applications
Abstract. Let A be an n by N real-valued matrix with n < N; we count the number of k-faces fk(AQ) when Q is either the standard N-dimensional hypercube IN or else the positive orthant RN +. To state results simply, consider a proportional-growth asymptotic, where for fixed δ, ρ in (0, 1), we have a sequence of matrices An,Nn and of integers kn with n/Nn → δ, kn/n → ρ as n → ∞. If each matrix An,Nn has its columns in general position, then fk(AIN)/fk(I N) tends to zero or one depending on whether ρ> min(0, 2 − δ−1) or ρ < min(0, 2 − δ−1). Also, if each An,Nn is a random draw from a distribution which is invariant under right multiplication by signed permutations, then fk(ARN +)/fk(RN +) tends almost surely to zero or one depending on whether ρ> min(0, 2 − δ−1) or ρ < min(0, 2 − δ−1). We make a variety of contrasts to related work on projections of the simplex and/or cross-polytope. These geometric face-counting results have implications for signal processing, information theory, inverse problems, and optimization. Indeed, face counting is related to conditions for uniqueness of solutions of underdetermine
Exploring causal networks underlying fat deposition and muscularity in pigs through the integration of phenotypic, genotypic and transcriptomic data
Genome Instability and Bleomicin Sensitivity Test
Procjena individualne osjetljivosti na mutagene često je dio istraživanja u epidemiološkim studijama koje prate pojavnost zloćudnih bolesti u populacijama. Posljedica djelovanja mutagena u genomu izloženih osoba jest nastanak određene, manje ili veće, količine oštećenja, uvjetovane individualnim razlikama u osjetljivosti. Viša razina takve genomske nestabilnosti znači opasnost (rizik) od razvoja zloćudnih bolesti.
Interindividualne razlike u odgovoru na mutagene obično se povezuju i s promijenjenom (većinom smanjenom) sposobnosti (kapacitetom) za popravak DNA. Citogenetičke studije su pokazale da je genom tumorskih stanica nestabilniji od normalnih, a time i skloniji akumuliranju oštećenja, bilo da je nestabilnost uzrokovana nasljeđem, izloženošću ili kombinacijom tih dvaju učinaka. U oboljelih ispitanika utvrđena je povećana učestalost kromatidnih i kromosomskih aberacija naspram normalne populacije te sklonost
razvoju određenih vrsta neoplazija. U praćenju povezanosti promijenjenog odgovora i pojavnosti tumora služe nam različiti biomarkeri. Kao indirektni pokazatelji uspješnosti popravka DNA često se rabe testovi osjetljivosti na mutagene u kulturama limfocita periferne krvi. Jedan od takvih testova je i bleomicinski
test. Radiomimetik i citostatik, a po strukturi glikopeptid, bleomicin se u stanici prevodi u aktivni oblik sposoban cijepati molekulu DNA što uzrokuje brojne jednolančane i dvolančane lomove. Kao jednostavna
i jeftina metoda, zasniva se na utvrđivanju ukupnog broja jednolančanih lomova u kromosomima limfocita uzgajanih u staničnoj kulturi koji su u uvjetima in vitro tijekom kasne G2-faze staničnog ciklusa bili izloženi bleomicinu. Ovaj revijalni rad daje pregled utjecaja raznih faktora na rezultate samog testa i pokazuje
njegovu široku primjenu u proučavanju genomske nestabilnosti koju najčešće uzrokuje kombinacija raznih faktora.Estimation of individual susceptibility to mutagens is often a part of epidemiological studies monitoring the appearance of malignant disease in different populations. Genome exposure to mutagens can lead to DNA damage. The rate of damage depends on individual differences in response, which are usually associated with differences in DNA repair capacity. Cytogenetic studies have shown that the genome of tumour cells is less stable than normal cells and therefore accumulates more damage. Tumour patients show a higher
frequency of chromatid and chromosomal aberrations and a predisposition to certain types of tumours.
One of the common biomarkers used in monitoring tumour appearance and changed response to DNA damage is the bleomycin test. In its active form, bleomycin (glycopeptid) is a radiomimetic cytostatic that can damage the DNA molecule and cause multiple single and double strands. The bleomycin test is simple and inexpensive, and is based on scoring chromatid breaks in lymphocytes in vitro exposed to bleomycin during the late G2 phase of the cell cycle. This review looks into different factors that may
affect test results and discusses its wide implementation in studies of genome instability usually caused by a combination of factors