When are fish sources versus sinks of nutrients in lake ecosystems?

Animals can be important in nutrient cycling through a variety of direct and indirect pathways. A high biomass of animals often represents a large pool of nutrients, leading some ecologists to argue that animal assemblages can represent nutrient sinks within ecosystems. The role of animals as sources vs. sinks of nutrients has been debated particularly extensively for freshwater fishes. We argue that a large pool size does not equate to a nutrient sink; rather, animals can be nutrient sinks when their biomass increases, when emigration rates are high, and/or when nutrients in animal carcasses are not remineralized. To further explore these ideas, we use a simple model to evaluate the conditions under which fish are phosphorus (P) sources or sinks at the ecosystem (lake) level, and at the habitat level (benthic and water column habitats). Our simulations suggest that, under most conditions, fish are sinks for benthic P but are net P sources to the water column. However, P source and sink strengths depend on fish feeding habits (proportion of P consumed from the benthos and water column), migration patterns, and especially the fate of carcass P. Of particular importance is the rate at which carcasses are mineralized and the relative importance of benthic vs. pelagic primary producers in taking up mineralized P (and excreted P). Higher proportional uptake of P by benthic primary producers increases the likelihood that fish are sinks for water column P. Carcass bones and scales are relatively recalcitrant and can represent a P sink even if fish biomass does not change over time. Thus, there is a need for better documentation of the fraction of carcass P that is remineralized, and the fate of this P, under natural conditions. We urge a more holistic perspective regarding the role of animals in nutrient cycling, with a focus on quantifying the rates at which animals consume, store, release, and transport nutrients under various conditions

Balancing problems in acyclic networks

A directed acyclic network with nonnegative integer arc lengths is called balanced if any two paths with common endpoints have equal lengths. In the buffer assignment problem such a network is given, and the goal is to balance it by increasing arc lengths by integer amounts (called buffers), so that the sum of the amounts added is minimal. This problem arises in VLSI design, and was recently shown to be polynomial for rooted networks. Here we give simple procedures which solve several generalizations of this problem in strongly polynomial time, using ideas from network flow theory. In particular, we solve a weighted version of the problem, extend the results to nonrooted networks, and allow upper bounds on buffers. We also give a strongly polynomial algorithm for solving the min-max buffer assignment problem, based on a strong proximity result between fractional and integer balanced solutions. Finally, we show that the problem of balancing a network while minimizing the number of arcs with positive buffers is NP-hard

A max-flow approach to improved lower bounds for quadratic unconstrained binary optimization (QUBO)

AbstractThe “roof dual” of a QUBO (Quadratic Unconstrained Binary Optimization) problem has been introduced in [P.L. Hammer, P. Hansen, B. Simeone, Roof duality, complementation and persistency in quadratic 0–1 optimization, Mathematical Programming 28 (1984) 121–155]; it provides a bound to the optimum value, along with a polynomial test of the sharpness of this bound, and (due to a “persistency” result) it also determines the values of some of the variables at the optimum. In this paper we provide a graph-theoretic approach to provide bounds, which includes as a special case the roof dual bound, and show that these bounds can be computed in O(n3) time by using network flow techniques. We also obtain a decomposition theorem for quadratic pseudo-Boolean functions, improving the persistency result of [P.L. Hammer, P. Hansen, B. Simeone, Roof duality, complementation and persistency in quadratic 0–1 optimization, Mathematical Programming 28 (1984) 121–155]. Finally, we show that the proposed bounds (including roof duality) can be applied in an iterated way to obtain significantly better bounds. Computational experiments on problems up to thousands of variables are presented

Immunotherapy with myeloid cells for tolerance induction

PURPOSE OF REVIEW: Understanding the interplay between myeloid dendritic cells and T cells under tolerogenic conditions, and whether their interactions induce the development of antigen-specific regulatory T cells (Tregs) is critical to uncover the mechanisms involved in the induction of indefinite allograft survival. RECENT FINDINGS: Myeloid dendritic cell-T-cell interactions are seminal events that determine the outcome of the immune response, and multiple in-vitro protocols suggest the generation of tolerogenic myeloid dendritic cells that modulate T-cell responses, and determine the outcome of the immune response to an allograft following adoptive transfer. We believe that identifying specific conditions that lead to the generation of tolerogenic myeloid dendritic cells and Tregs are critical for the manipulation of the immune response towards the development of transplantation tolerance. SUMMARY: We summarize recent findings regarding specific culture conditions that generate tolerogenic myeloid dendritic cells that induce T-cell hyporesponsiveness and Treg development, which represents a novel immunotherapeutic approach to promote the induction of indefinite graft survival prolongation. The interpretations presented here illustrate that different mechanisms govern the generation of tolerogenic myeloid dendritic cells, and we discuss the concomitant therapeutic implications.This work was supported by the Programa Ramón y Cajal RYC-2006-1588, Ministerio de Educa-ción y Ciencia SAF2007-63579, Programa José Castillejo JC2008-00065, and Programa de Investigación de Grupos Emergentes del ISCIII (to J.C.O.), and NIH R01 AI-41428, AI-72039, and the Emerald Foundation (to J.S.B.).S

Correction of bleeding in experimental severe hemophilia A by systemic delivery of factor VIII- encoding mRNA Short title: mRNA-based therapy for hemophilia A Scientific category: Thrombosis and Hemostasis

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Human p53 interacts with the elongating RNAPII complex and is required for the release of actinomycin D induced transcription blockage

The p53 tumour suppressor regulates the transcription initiation of selected genes by binding to specific DNA sequences at their promoters. Here we report a novel role of p53 in transcription elongation in human cells. Our data demonstrate that upon transcription elongation blockage, p53 is associated with genes that have not been reported as its direct targets. p53 could be co-immunoprecipitated with active forms of DNA-directed RNA polymerase II subunit 1 (RPB1), highlighting its association with the elongating RNA polymerase II. During a normal transcription cycle, p53 and RPB1 are localised at distinct regions of selected non-canonical p53 target genes and this pattern of localisation was changed upon blockage of transcription elongation. Additionally, transcription elongation blockage induced the proteasomal degradation of RPB1. Our results reveal a novel role of p53 in human cells during transcription elongation blockage that may facilitate the removal of RNA polymerase II from DNA

Human p53 interacts with the elongating RNAPII complex and is required for the release of actinomycin D induced transcription blockage

The p53 tumour suppressor regulates the transcription initiation of selected genes by binding to specific DNA sequences at their promoters. Here we report a novel role of p53 in transcription elongation in human cells. Our data demonstrate that upon transcription elongation blockage, p53 is associated with genes that have not been reported as its direct targets. p53 could be co-immunoprecipitated with active forms of DNA-directed RNA polymerase II subunit 1 (RPB1), highlighting its association with the elongating RNA polymerase II. During a normal transcription cycle, p53 and RPB1 are localised at distinct regions of selected non-canonical p53 target genes and this pattern of localisation was changed upon blockage of transcription elongation. Additionally, transcription elongation blockage induced the proteasomal degradation of RPB1. Our results reveal a novel role of p53 in human cells during transcription elongation blockage that may facilitate the removal of RNA polymerase II from DNA

Genomic analysis of a novel picornavirus from a migratory waterfowl, greater white-fronted goose (Anser albifrons)

The complete genome of goose picornavirus 1 (GPV-1) strain goose/NLSZK2/HUN/2013 (MF358731) was determined by RT-PCR and next-generation sequencing from a cloacal sample of a migratory waterfowl, greater white-fronted goose (Anser albifrons) in Hungary. The genome of GPV-1 shows an L-3-3-4 organization pattern with a 5'-terminal origin of replication (ORI) region, a type-IV IRES, and an Hbox/NC-type 2A protein. This virus showed the highest overall sequence identity to the members of the genus Kobuvirus, although the phylogenetic position of GPV-1 is different in the analyzed P1, 2C and 3CD phylogenetic trees, which further increases the diversity of known avian picornaviruses