1,319 research outputs found
The phonon Boltzmann equation, properties and link to weakly anharmonic lattice dynamics
For low density gases the validity of the Boltzmann transport equation is
well established. The central object is the one-particle distribution function,
, which in the Boltzmann-Grad limit satisfies the Boltzmann equation. Grad
and, much refined, Cercignani argue for the existence of this limit on the
basis of the BBGKY hierarchy for hard spheres. At least for a short kinetic
time span, the argument can be made mathematically precise following the
seminal work of Lanford. In this article a corresponding programme is
undertaken for weakly nonlinear, both discrete and continuum, wave equations.
Our working example is the harmonic lattice with a weakly nonquadratic on-site
potential. We argue that the role of the Boltzmann -function is taken over
by the Wigner function, which is a very convenient device to filter the slow
degrees of freedom. The Wigner function, so to speak, labels locally the
covariances of dynamically almost stationary measures. One route to the phonon
Boltzmann equation is a Gaussian decoupling, which is based on the fact that
the purely harmonic dynamics has very good mixing properties. As a further
approach the expansion in terms of Feynman diagrams is outlined. Both methods
are extended to the quantized version of the weakly nonlinear wave equation.
The resulting phonon Boltzmann equation has been hardly studied on a rigorous
level. As one novel contribution we establish that the spatially homogeneous
stationary solutions are precisely the thermal Wigner functions. For three
phonon processes such a result requires extra conditions on the dispersion law.
We also outline the reasoning leading to Fourier's law for heat conduction.Comment: special issue on "Kinetic Theory", Journal of Statistical Physics,
improved versio
Prenatal Lead Levels, Plasma Amyloid β Levels, and Gene Expression in Young Adulthood
Background: Animal studies suggest that early-life lead exposure influences gene expression and production of proteins associated with Alzheimer’s disease (AD)
Maternal Particulate Matter Exposure Impairs Lung Health and Is Associated with Mitochondrial Damage.
Relatively little is known about the transgenerational effects of chronic maternal exposure to low-level traffic-related air pollution (TRAP) on the offspring lung health, nor are the effects of removing such exposure before pregnancy. Female BALB/c mice were exposed to PM2.5 (PM2.5, 5 µg/day) for 6 weeks before mating and during gestation and lactation; in a subgroup, PM was removed when mating started to model mothers moving to cleaner areas during pregnancy to protect their unborn child (Pre-exposure). Lung pathology was characterised in both dams and offspring. A subcohort of female offspring was also exposed to ovalbumin to model allergic airways disease. PM2.5 and Pre-exposure dams exhibited airways hyper-responsiveness (AHR) with mucus hypersecretion, increased mitochondrial reactive oxygen species (ROS) and mitochondrial dysfunction in the lungs. Female offspring from PM2.5 and Pre-exposure dams displayed AHR with increased lung inflammation and mitochondrial ROS production, while males only displayed increased lung inflammation. After the ovalbumin challenge, AHR was increased in female offspring from PM2.5 dams compared with those from control dams. Using an in vitro model, the mitochondria-targeted antioxidant MitoQ reversed mitochondrial dysfunction by PM stimulation, suggesting that the lung pathology in offspring is driven by dysfunctional mitochondria. In conclusion, chronic exposure to low doses of PM2.5 exerted transgenerational impairment on lung health
ISU201 Enhances the Resolution of Airway Inflammation in a Mouse Model of an Acute Exacerbation of Asthma
Smc5/6 coordinates formation and resolution of joint molecules with chromosome morphology to ensure meiotic divisions
During meiosis, Structural Maintenance of Chromosome (SMC) complexes underpin two fundamental features of meiosis: homologous recombination and chromosome segregation. While meiotic functions of the cohesin and condensin complexes have been delineated, the role of the third SMC complex, Smc5/6, remains enigmatic. Here we identify specific, essential meiotic functions for the Smc5/6 complex in homologous recombination and the regulation of cohesin. We show that Smc5/6 is enriched at centromeres and cohesin-association sites where it regulates sister-chromatid cohesion and the timely removal of cohesin from chromosomal arms, respectively. Smc5/6 also localizes to recombination hotspots, where it promotes normal formation and resolution of a subset of joint-molecule intermediates. In this regard, Smc5/6 functions independently of the major crossover pathway defined by the MutLγ complex. Furthermore, we show that Smc5/6 is required for stable chromosomal localization of the XPF-family endonuclease, Mus81-Mms4Eme1. Our data suggest that the Smc5/6 complex is required for specific recombination and chromosomal processes throughout meiosis and that in its absence, attempts at cell division with unresolved joint molecules and residual cohesin lead to severe recombination-induced meiotic catastroph
Not to normal order - Notes on the kinetic limit for weakly interacting quantum fluids
The derivation of the Nordheim-Boltzmann transport equation for weakly
interacting quantum fluids is a longstanding problem in mathematical physics.
Inspired by the method developed to handle classical dilute gases, a
conventional approach is the use of the BBGKY hierarchy for the time-dependent
reduced density matrices. In contrast, our contribution is motivated by the
kinetic theory of the weakly nonlinear Schrodinger equation. The main
observation is that the results obtained in the latter context carry over
directly to weakly interacting quantum fluids provided one does not insist on
normal order in the Duhamel expansion. We discuss the term by term convergence
of the expansion and the equilibrium time correlation .Comment: 43 pages, corrected typos, updated assumptions in sec.
The emergence and diversification of a zoonotic pathogen from within the microbiota of intensively farmed pigs
The expansion and intensification of livestock production is predicted to promote the
emergence of pathogens. As pathogens sometimes jump between species, this can affect
the health of humans as well as livestock. Here, we investigate how livestock microbiota
can act as a source of these emerging pathogens through analysis of Streptococcus suis, a
ubiquitous component of the respiratory microbiota of pigs that is also a major cause of
disease on pig farms and an important zoonotic pathogen. Combining molecular dating,
phylogeography, and comparative genomic analyses of a large collection of isolates, we
find that several pathogenic lineages of S. suis emerged in the 19th and 20th centuries,
during an early period of growth in pig farming. These lineages have since spread between
countries and continents, mirroring trade in live pigs. They are distinguished by the
presence of three genomic islands with putative roles in metabolism and cell adhesion,
and an ongoing reduction in genome size, which may reflect their recent shift to a more
pathogenic ecology. Reconstructions of the evolutionary histories of these islands reveal
constraints on pathogen emergence that could inform control strategies, with pathogenic lineages consistently emerging from one subpopulation of S. suis and acquiring
genes through horizontal transfer from other pathogenic lineages. These results shed
light on the capacity of the microbiota to rapidly evolve to exploit changes in their host
population and suggest that the impact of changes in farming on the pathogenicity and
zoonotic potential of S. suis is yet to be fully realized.This work was primarily funded by an EU Horizon 2020 grant “PIGSs” (727966) and a ZELS BBSRC award “Myanmar Pigs Partnership (MPP)” (BB/L018934/1). G.G.R.M., E.L.M., and L.A.W. were supported by a Sir Henry Dale Fellowship to L.A.W. jointly funded by the Wellcome Trust and the Royal Society (109385/Z/15/Z). N.H. was supported by a Challenge grant from the Royal Society (CH16011) and an Isaac Newton Trust Research Grant [17.24(u)]. G.G.R.M. was also supported by a Research Fellowship at Newnham College. S.B. is supported by the Medical Research Council (MR/V032836/1). PIC North America provided part of the funds for the sequencing of the isolates from the USA. A.J.B. and M.M. were funded by Medical Research Council and Biotechnology and Biological Sciences Research Council studentships respectively, and M.M. was co-funded by the Raymond and Beverly Sackler Fund. We would like to acknowledge Susanna Williamson at the APHA for providing samples, Oscar Cabezón for sampling of the wild boar population in Spain, Mark O’Dea for access to sequence data from Australian isolates, the PIGSs and MPP consortiums for providing samples and helpful discussions, Julian Parkhill and John Welch for helpful discussions, and two anonymous reviewers for their valuable suggestions for improving the manuscript. This research was funded in whole or in part by the Wellcome Trust. For the purpose of Open Access, the author has applied a CC BY public copyright license to any Author Accepted Manuscript (AAM) version arising from this submission.info:eu-repo/semantics/publishedVersio
Identification of novel vascular targets in lung cancer
Background: Lung cancer remains the leading cause of cancer-related death, largely owing to the lack of effective treatments.
A tumour vascular targeting strategy presents an attractive alternative; however, the molecular signature of the vasculature in lung
cancer is poorly explored. This work aimed to identify novel tumour vascular targets in lung cancer.
Methods: Enzymatic digestion of fresh tissue followed by endothelial capture with Ulex lectin-coated magnetic beads was used to
isolate the endothelium from fresh tumour specimens of lung cancer patients. Endothelial isolates from the healthy and tumour
lung tissue were subjected to whole human genome expression profiling using microarray technology.
Results: Bioinformatics analysis identified tumour endothelial expression of angiogenic factors, matrix metalloproteases and cellsurface
transmembrane proteins. Predicted novel tumour vascular targets were verified by RNA-seq, quantitative real-time PCR
analysis and immunohistochemistry. Further detailed expression profiling of STEAP1 on 82 lung cancer patients confirmed
STEAP1 as a novel target in the tumour vasculature. Functional analysis of STEAP1 using siRNA silencing implicates a role in
endothelial cell migration and tube formation.
Conclusions: The identification of cell-surface tumour endothelial markers in lung is of interest in therapeutic antibody and
vaccine development
The emergence and diversification of a zoonotic pathogen from within the microbiota of intensively farmed pigs
The expansion and intensification of livestock production is predicted to promote the emergence of pathogens. As pathogens sometimes jump between species, this can affect the health of humans as well as livestock. Here, we investigate how livestock microbiota can act as a source of these emerging pathogens through analysis of Streptococcus suis, a ubiquitous component of the respiratory microbiota of pigs that is also a major cause of disease on pig farms and an important zoonotic pathogen. Combining molecular dating, phylogeography, and comparative genomic analyses of a large collection of isolates, we find that several pathogenic lineages of S. suis emerged in the 19th and 20th centuries, during an early period of growth in pig farming. These lineages have since spread between countries and continents, mirroring trade in live pigs. They are distinguished by the presence of three genomic islands with putative roles in metabolism and cell adhesion, and an ongoing reduction in genome size, which may reflect their recent shift to a more pathogenic ecology. Reconstructions of the evolutionary histories of these islands reveal constraints on pathogen emergence that could inform control strategies, with pathogenic lineages consistently emerging from one subpopulation of S. suis and acquiring genes through horizontal transfer from other pathogenic lineages. These results shed light on the capacity of the microbiota to rapidly evolve to exploit changes in their host population and suggest that the impact of changes in farming on the pathogenicity and zoonotic potential of S. suis is yet to be fully realized
Theoretical Analysis of the Stress Induced B-Z Transition in Superhelical DNA
We present a method to calculate the propensities of regions within a DNA molecule to transition from B-form to Z-form under negative superhelical stresses. We use statistical mechanics to analyze the competition that occurs among all susceptible Z-forming regions at thermodynamic equilibrium in a superhelically stressed DNA of specified sequence. This method, which we call SIBZ, is similar to the SIDD algorithm that was previously developed to analyze superhelical duplex destabilization. A state of the system is determined by assigning to each base pair either the B- or the Z-conformation, accounting for the dinucleotide repeat unit of Z-DNA. The free energy of a state is comprised of the nucleation energy, the sequence-dependent B-Z transition energy, and the energy associated with the residual superhelicity remaining after the change of twist due to transition. Using this information, SIBZ calculates the equilibrium B-Z transition probability of each base pair in the sequence. This can be done at any physiologically reasonable level of negative superhelicity. We use SIBZ to analyze a variety of representative genomic DNA sequences. We show that the dominant Z-DNA forming regions in a sequence can compete in highly complex ways as the superhelicity level changes. Despite having no tunable parameters, the predictions of SIBZ agree precisely with experimental results, both for the onset of transition in plasmids containing introduced Z-forming sequences and for the locations of Z-forming regions in genomic sequences. We calculate the transition profiles of 5 kb regions taken from each of 12,841 mouse genes and centered on the transcription start site (TSS). We find a substantial increase in the frequency of Z-forming regions immediately upstream from the TSS. The approach developed here has the potential to illuminate the occurrence of Z-form regions in vivo, and the possible roles this transition may play in biological processes
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