1,036 research outputs found
The Differential Form Method for Finding Symmetries
This article reviews the use of differential forms and Lie derivatives to
find symmetries of differential equations, as originally presented by Harrison
and Estabrook, J. Math. Phys., 12 (1971), 653. An outline of the method is
given, followed by examples and references to recent papers using the method.Comment: Published in SIGMA (Symmetry, Integrability and Geometry: Methods and
Applications) at http://www.emis.de/journals/SIGMA
A Method for Constructing a Lax Pair for the Ernst Equation
A systematic construction of a Lax pair and an infinite set of conservation
laws for the Ernst equation is described. The matrix form of this equation is
rewritten as a differential ideal of gl(2,R)-valued differential forms, and its
symmetry condition is expressed as an exterior equation which is linear in the
symmetry characteristic and has the form of a conservation law. By means of a
recursive process, an infinite collection of such laws is then obtained, and
the conserved "charges" are used to derive a linear exterior equation whose
components constitute a Lax pair.Comment: 12 pages; minor correction
Mitigation measures to reduce entanglements of migrating whales with commercial fishing gear
The West Coast Rock Lobster Managed Fishery (WCRLMF) transitioned to a quota based fishery, and year-round fishing, which corresponded with a spike in whale entanglements in 2013. This presented industry with a challenging social issue, to reduce entanglements without impacting on the financial benefits that the shift to year-round quota fishing had afforded
Latitudinal dependency of geomagnetic polarity transition durations
Palaeomagnetic records of the Matuyama-Brunhes polarity transition were obtained from seven, low sedimentation rate, deepsea cores from the Pacific Ocean. The cores were taken near the 180° meridian and provide a latitudinal transect of transition records extending from 45.3° N to 33.4° S. Examination of these records suggests that low sedimentation rate cores may not be capable of recording the fine details of transitional field behaviour, but there are indications that these cores may, in fact, provide accurate records of the more general features of the reversal. Most notable of these features is that the duration of the transition is dependent on the site latitude, with durations at mid-latitudes being more than a factor of 2 longer than at equatorial latitudes
Poor People’s Politics in East Timor
YesPoor people attempting to claim a share of resources in post-conflict societies seek allies internationally and nationally in attempts to empower their campaigns. In so doing, they mobilize the languages of liberalism, nationalism and local cultural tradition selectively and opportunistically to both justify stances that transgress the strictures of local culture and to cement alliances with more powerful actors. In the case of poor widows in East Timor, the languages of nationalism, ritual, and justice were intermingled in a campaign aimed at both international actors and the national state in a bid to claim a position of status in the post-conflict order
Classical and quantum: a conflict of interest
We highlight three conflicts between quantum theory and classical general
relativity, which make it implausible that a quantum theory of gravity can be
arrived at by quantising classical gravity. These conflicts are: quantum
nonlocality and space-time structure; the problem of time in quantum theory;
and the quantum measurement problem. We explain how these three aspects bear on
each other, and how they point towards an underlying noncommutative geometry of
space-time.Comment: 15 pages. Published in `Gravity and the quantum' [Essays in honour of
Thanu Padmanabhan on the occasion of his sixtieth birthday] Eds. Jasjeet
Singh Bagla and Sunu Engineer (Springer, 2017
The Two Different Isoforms of the RSC Chromatin Remodeling Complex Play Distinct Roles in DNA Damage Responses
The RSC chromatin remodeling complex has been implicated in contributing to DNA double-strand break (DSB) repair in a number of studies. Both survival and levels of H2A phosphorylation in response to damage are reduced in the absence of RSC. Importantly, there is evidence for two isoforms of this complex, defined by the presence of either Rsc1 or Rsc2. Here, we investigated whether the two isoforms of RSC provide distinct contributions to DNA damage responses. First, we established that the two isoforms of RSC differ in the presence of Rsc1 or Rsc2 but otherwise have the same subunit composition. We found that both rsc1 and rsc2 mutant strains have intact DNA damage-induced checkpoint activity and transcriptional induction. In addition, both strains show reduced non-homologous end joining activity and have a similar spectrum of DSB repair junctions, suggesting perhaps that the two complexes provide the same functions. However, the hypersensitivity of a rsc1 strain cannot be complemented with an extra copy of RSC2, and likewise, the hypersensitivity of the rsc2 strain remains unchanged when an additional copy of RSC1 is present, indicating that the two proteins are unable to functionally compensate for one another in DNA damage responses. Rsc1, but not Rsc2, is required for nucleosome sliding flanking a DNA DSB. Interestingly, while swapping the domains from Rsc1 into the Rsc2 protein does not compromise hypersensitivity to DNA damage suggesting they are functionally interchangeable, the BAH domain from Rsc1 confers upon Rsc2 the ability to remodel chromatin at a DNA break. These data demonstrate that, despite the similarity between Rsc1 and Rsc2, the two different isoforms of RSC provide distinct functions in DNA damage responses, and that at least part of the functional specificity is dictated by the BAH domains
Longitudinal Cytokine Profiling Identifies GRO-α and EGF as Potential Biomarkers of Disease Progression in Essential Thrombocythemia.
Myeloproliferative neoplasms (MPNs) are characterized by deregulation of mature blood cell production and increased risk of myelofibrosis (MF) and leukemic transformation. Numerous driver mutations have been identified but substantial disease heterogeneity remains unexplained, implying the involvement of additional as yet unidentified factors. The inflammatory microenvironment has recently attracted attention as a crucial factor in MPN biology, in particular whether inflammatory cytokines and chemokines contribute to disease establishment or progression. Here we present a large-scale study of serum cytokine profiles in more than 400 MPN patients and identify an essential thrombocythemia (ET)-specific inflammatory cytokine signature consisting of Eotaxin, GRO-α, and EGF. Levels of 2 of these markers (GRO-α and EGF) in ET patients were associated with disease transformation in initial sample collection (GRO-α) or longitudinal sampling (EGF). In ET patients with extensive genomic profiling data (n = 183) cytokine levels added significant prognostic value for predicting transformation from ET to MF. Furthermore, CD56+CD14+ pro-inflammatory monocytes were identified as a novel source of increased GRO-α levels. These data implicate the immune cell microenvironment as a significant player in ET disease evolution and illustrate the utility of cytokines as potential biomarkers for reaching beyond genomic classification for disease stratification and monitoring.The serum cytokine studies were supported by a research grant from the Rosetrees Trust. NFØ was supported by grants from the Danish Lundbeck Foundation and Danish Cancer Society, J.G. was supported by fellowships from Bloodwise and the Kay Kendall Leukaemia Fund; and M.S.S. is the recipient of a Biotechnology and Biological Sciences Research Council Industrial Collaborative Awards in Science and Engineering PhD Studentship. Work in the R.C.S. laboratory was supported by grants from the Stiftung Blutspendezentrum SRK beider Basel, the Swiss National Science Foundation (31003A-147016/1 and 31003A_166613), and the Swiss Cancer League (KLS-2950-02-2012 and KFS-3655-02-2015). A.K. was supported by the Else Kröner-Fresenius Foundation. Work in the A.R.G. laboratory is supported by the Wellcome Trust, Bloodwise, Cancer Research UK, the Kay Kendall Leukaemia Fund, and the Leukemia and Lymphoma Society of America. Work in the D.G.K. laboratory is supported by a Bloodwise Bennett Fellowship (15008), a European Hematology Association Non-Clinical Advanced Research Fellowship, and an ERC Starting Grant (ERC-2016-STG–715371). D.G.K. and A.R.G. are supported by a core support grant from the Wellcome Trust and Medical Research Council to the Wellcome MRC Cambridge Stem Cell Institute, the National Institute for Health Research Cambridge Biomedical Research Centre, and the CRUK Cambridge Cancer Centre
Segmental duplications in the human genome reveal details of pseudogene formation
Duplicated pseudogenes in the human genome are disabled copies of functioning parent genes. They result from block duplication events occurring throughout evolutionary history. Relatively recent duplications (with sequence similarity ≥90% and length ≥1 kb) are termed segmental duplications (SDs); here, we analyze the interrelationship of SDs and pseudogenes. We present a decision-tree approach to classify pseudogenes based on their (and their parents’) characteristics in relation to SDs. The classification identifies 140 novel pseudogenes and makes possible improved annotation for the 3172 pseudogenes located in SDs. In particular, it reveals that many pseudogenes in SDs likely did not arise directly from parent genes, but are the result of a multi-step process. In these cases, the initial duplication or retrotransposition of a parent gene gives rise to a ‘parent pseudogene’, followed by further duplication creating duplicated–duplicated or duplicated–processed pseudogenes, respectively. Moreover, we can precisely identify these parent pseudogenes by overlap with ancestral SD loci. Finally, a comparison of nucleotide substitutions per site in a pseudogene with its surrounding SD region allows us to estimate the time difference between duplication and disablement events, and this suggests that most duplicated pseudogenes in SDs were likely disabled around the time of the original duplication
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