116 research outputs found

    Deriving observation distances for camera trap distance sampling

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    Camera trap distance sampling (CTDS)o is a recently developed survey method to estimate animal abundance from camera trap data for unmarked populations. It re-quires the estimation of camera-animal observation distances, which previously was done by comparing animal positions to reference labels at predefined intervals. Here, we test a photogrammetry approach to derive camera-animal observation distances. We applied both, the reference label and photogrammetry approaches to five un-gulate species varying widely in body size (Giraffa camelopardalis, Equus grevyi, Oryx dammah, Kobus megaceros and Eudorcas thomsonii) and one ground-dwelling bird spe-cies (Numida meleagris) inhabiting a large enclosure and estimated their density with CTDS. Both procedures provided highly correlated observation distances (ρ= 0.99, pCTDS en anglais) est une technique de recensement dĂ©veloppĂ©e rĂ©cemment qui permet d’estimer l’effectif de populations animales non marquĂ©es avec des piĂšges photographiques. Cette technique requiert l’estimation de la distance entre le piĂšge photographique et l’animal observĂ©, ce qui Ă©tait prĂ©cĂ©demment obtenu en comparant la position de l’animal Ă  des points de rĂ©fĂ©rence placĂ©s Ă  des intervalles prĂ©dĂ©finis. Ici nous testons une approche de photogrammĂ©trie pour estimer les distances entre les piĂšges photographiques et les animaux observĂ©s. Nous avons appliquĂ© les deux approches, points de rĂ©fĂ©rence et photogrammĂ©tries, Ă  cinq espĂšces d’ongulĂ©s de tailles diffĂ©rentes (Giraffa camelopardalis, Equus grevyi, Oryx dammah, Kobus megaceros et Eudorcas thomsonii) ainsi qu’une espĂšce d’oiseau (Numida meleagris) vivant dans un espace clĂŽturĂ© et avons estimĂ© leur densitĂ©s de populations avec le CTDS. Les deux mĂ©thodes ont fourni des distances d’observations fortement corrĂ©lĂ©es (ρ = 0.99, p significative pour la technique de photogrammĂ©trie (MD = 0.28 m, p est nĂ©anmoins nĂ©gligeable dans la mesure oĂč, pour les analyses, les distances Ă©taient groupĂ©es dans des intervalles allant de 2 Ă  5 mĂštres. En rĂšgle gĂ©nĂ©rale, les estimations d’abondances Ă©taient proche du nombre rĂ©el d’individus dans l’enclos, et ce pour les deux techniques, avec l’exception des zĂšbres pour lesquels les densitĂ©s Ă©taient sous- estimĂ©es. La technique de photogrammĂ©trie offre une alternative pour dĂ©river les distances entre les piĂšges photographiques et les animaux observĂ©s et pourrait ĂȘtre particuliĂšrement utile dans des habitats ouverts oĂč les animaux sont peu cachĂ©s

    Specific nuclear envelope transmembrane proteins can promote the location of chromosomes to and from the nuclear periphery

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    BACKGROUND: Different cell types have distinctive patterns of chromosome positioning in the nucleus. Although ectopic affinity-tethering of specific loci can be used to relocate chromosomes to the nuclear periphery, endogenous nuclear envelope proteins that control such a mechanism in mammalian cells have yet to be widely identified. RESULTS: To search for such proteins twenty three nuclear envelope transmembrane proteins were screened for their ability to promote peripheral localization of human chromosomes in HT1080 fibroblasts. Five of these proteins had strong effects on chromosome 5, but individual proteins affected different subsets of chromosomes. The repositioning effects were reversible and the proteins with effects all exhibited highly tissue-restricted patterns of expression. Depletion of two nuclear envelope transmembrane proteins that were preferentially expressed in liver each reduced the normal peripheral positioning of chromosome 5 in liver cells. CONCLUSIONS: The discovery of nuclear envelope transmembrane proteins that can modulate chromosome position and have restricted patterns of expression may enable dissection of the functional relevance of tissue-specific patterns of radial chromosome positioning.Publisher PDFPeer reviewe

    Synthesis and characterization of nanocrystalline U1−x_{1-x}Pux_{x}O2(+y)_{2(+y)} mixed oxides

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    We report here the first synthesis of mixed oxide U1−x_{1-x}Pux_{x}O2(+y)_{2(+y)} nanoparticles. The obtained nanopowders were characterized by X-ray diffraction, thermal ionization mass spectrometry, transmission electron microscopy, Raman spectroscopy, and U M4_{4} edge high-energy-resolution X-ray absorption near edge structure (HR-XANES). The HR-XANES spectra give evidence for the partial oxidation of UIV^{IV} to UV^{V}. This novel route toward the formation of actinide–actinide solid solution opens research opportunities that are not accessible using bulk materials. We give details on the X-ray diffraction study on plutonium oxalate hexahydrate, as a reagent for the synthesis of such nanoparticles

    Alternating runtime and size complexity analysis of integer programs

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    We present a modular approach to automatic complexity analysis. Based on a novel alternation between finding symbolic time bounds for program parts and using these to infer size bounds on program variables, we can restrict each analysis step to a small part of the program while maintaining a high level of precision. Extensive experiments with the implementation of our method demonstrate its performance and power in comparison with other tools

    NET23/STING promotes chromatin compaction from the nuclear envelope

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    Changes in the peripheral distribution and amount of condensed chromatin are observed in a number of diseases linked to mutations in the lamin A protein of the nuclear envelope. We postulated that lamin A interactions with nuclear envelope transmembrane proteins (NETs) that affect chromatin structure might be altered in these diseases and so screened thirty-one NETs for those that promote chromatin compaction as determined by an increase in the number of chromatin clusters of high pixel intensity. One of these, NET23 (also called STING, MITA, MPYS, ERIS, Tmem173), strongly promoted chromatin compaction. A correlation between chromatin compaction and endogenous levels of NET23/STING was observed for a number of human cell lines, suggesting that NET23/STING may contribute generally to chromatin condensation. NET23/STING has separately been found to be involved in innate immune response signaling. Upon infection cells make a choice to either apoptose or to alter chromatin architecture to support focused expression of interferon genes and other response factors. We postulate that the chromatin compaction induced by NET23/STING may contribute to this choice because the cells expressing NET23/STING eventually apoptose, but the chromatin compaction effect is separate from this as the condensation was still observed when cells were treated with Z-VAD to block apoptosis. NET23/STING-induced compacted chromatin revealed changes in epigenetic marks including changes in histone methylation and acetylation. This indicates a previously uncharacterized nuclear role for NET23/STING potentially in both innate immune signaling and general chromatin architecture

    SL-COMP: Competition of Solvers for Separation Logic

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    International audienceSL-COMP aims at bringing together researchers interested on improving the state of the art of the automated deduction methods for Separation Logic (SL). The event took place twice until now and collected more than 1K problems for different fragments of SL. The input format of problems is based on the SMT-LIB format and therefore fully typed; only one new command is added to SMT-LIB's list, the command for the declaration of the heap's type. The SMT-LIB theory of SL comes with ten logics, some of them being combinations of SL with linear arithmetics. The competition's divisions are defined by the logic fragment, the kind of decision problem (satisfiability or entailment) and the presence of quantifiers. Until now, SL-COMP has been run on the StarExec platform, where the benchmark set and the binaries of participant solvers are freely available. The benchmark set is also available with the competition's documentation on a public repository in GitHub

    Activation of natural regulatory T cells by IgG Fc-derived peptide Tregitopes

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    We have identified at least 2 highly promiscuous major histocompatibility complex class II T-cell epitopes in the Fc fragment of IgG that are capable of specifically activating CD4+CD25HiFoxP3+ natural regulatory T cells (nTRegs). Coincubation of these regulatory T-cell epitopes or “Tregitopes” and antigens with peripheral blood mononuclear cells led to a suppression of effector cytokine secretion, reduced proliferation of effector T cells, and caused an increase in cell surface markers associated with TRegs such as FoxP3. In vivo administration of the murine homologue of the Fc region Tregitope resulted in suppression of immune response to a known immunogen. These data suggest that one mechanism for the immunosuppressive activity of IgG, such as with IVIG, may be related to the activity of regulatory T cells. In this model, regulatory T-cell epitopes in IgG activate a subset of nTRegs that tips the resulting immune response toward tolerance rather than immunogenicity

    Role of breast regression protein 39 (BRP-39)/chitinase 3-like-1 in Th2 and IL-13–induced tissue responses and apoptosis

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    Mouse breast regression protein 39 (BRP-39; Chi3l1) and its human homologue YKL-40 are chitinase-like proteins that lack chitinase activity. Although YKL-40 is expressed in exaggerated quantities and correlates with disease activity in asthma and many other disorders, the biological properties of BRP-39/YKL-40 have only been rudimentarily defined. We describe the generation and characterization of BRP-39−/− mice, YKL-40 transgenic mice, and mice that lack BRP-39 and produce YKL-40 only in their pulmonary epithelium. Studies of these mice demonstrated that BRP-39−/− animals have markedly diminished antigen-induced Th2 responses and that epithelial YKL-40 rescues the Th2 responses in these animals. The ability of interleukin13 to induce tissue inflammation and fibrosis was also markedly diminished in the absence of BRP-39. Mechanistic investigations demonstrated that BRP-39 and YKL-40 play an essential role in antigen sensitization and immunoglobulin E induction, stimulate dendritic cell accumulation and activation, and induce alternative macrophage activation. These proteins also inhibit inflammatory cell apoptosis/cell death while inhibiting Fas expression, activating protein kinase B/AKT, and inducing Faim 3. These studies establish novel regulatory roles for BRP-39/YKL-40 in the initiation and effector phases of Th2 inflammation and remodeling and suggest that these proteins are therapeutic targets in Th2- and macrophage-mediated disorders

    Nuclear envelope protein Lem2 is required for mouse development and regulates MAP and AKT kinases

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    The nuclear lamina, along with associated nuclear membrane proteins, is a nexus for regulating signaling in the nucleus. Numerous human diseases arise from mutations in lamina proteins, and experimental models for these disorders have revealed aberrant regulation of various signaling pathways. Previously, we reported that the inner nuclear membrane protein Lem2, which is expressed at high levels in muscle, promotes the differentiation of cultured myoblasts by attenuating ERK signaling. Here, we have analyzed mice harboring a disrupted allele for the Lem2 gene (Lemd2). No gross phenotypic defects were seen in heterozygotes, although muscle regeneration induced by cardiotoxin was delayed. By contrast, homozygous Lemd2 knockout mice died by E11.5. Although many normal morphogenetic hallmarks were observed in E10.5 knockout embryos, most tissues were substantially reduced in size. This was accompanied by activation of multiple MAP kinases (ERK1/2, JNK, p38) and AKT. Knockdown of Lem2 expression in C2C12 myoblasts also led to activation of MAP kinases and AKT. These findings indicate that Lemd2 plays an essential role in mouse embryonic development and that it is involved in regulating several signaling pathways. Since increased MAP kinase and AKT/mTORC signaling is found in other animal models for diseases linked to nuclear lamina proteins, LEMD2 should be considered to be another candidate gene for human disease
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