103,107 research outputs found
Data, R Code, and Output Supporting: Evaluating species-specific responses to camera-trap survey designs
No full textThese files contain data, R code and associated output supporting results presented in "Iannarilli, F., Erb, J., Arnold, T. W., and Fieberg, J. R. (2020). Evaluating species-specific responses to camera-trap survey designs. Wildlife Biology". In this paper, we assess species-specific responses by ten medium-to-large North-American carnivores to different survey design strategies commonly applied in camera-trap studies. Data were collected in northern Minnesota, USA, between 2016 and 2018 (23 337 active trap-days). We compared responses to: 1) two different survey-design frameworks (random- versus road-based), 2) two different lure types (salmon oil versus fatty acid scent oil), 3) two different placement strategies (completely random versus randomly-selected sites with feature-based placement), 4) survey timing (spring versus fall) and 5) temporal trends in daily encounter probabilities. Our results show that even species morphologically and taxonomically similar respond differently to survey-design strategies, and, thus, species-specific responses to design choices should be carefully considered in camera trap studies focused on multiple species.Minnesota Department of Natural ResourcesWildlife Restoration Program (Pittman- Robertson)Iannarilli, Fabiola; Erb, John; Arnold, Todd, W; Fieberg, John R. (2020). Data, R Code, and Output Supporting: Evaluating species-specific responses to camera-trap survey designs. Retrieved from the University Digital Conservancy, https://doi.org/10.13020/97b4-jh36
Besser als die Natur
No full textDer Biologe Tobias Erb hat es geschafft, den Prozess der Photosynthese effektiver zu machen. Zumindest im Reagenzglas funktioniert es
A Novel Fully Human Antitumor ImmunoRNase Targeting ErbB2-Positive Tumors
No full textA second generation anti-ErbB2 ImmunoRNase, called Erb-hcAb-RNase, was obtained by the fusion of Erb-hcAb, a human compact anti-ErbB2 antibody, with human pancreatic ribonuclease (HP-RNase or RNase 1).
We show herein that Erb-hcAb-RNase retains the enzymatic activity of human pancreatic RNase and specifically binds to ErbB2-positive cells with an affinity comparable to that of the parental Erb-hcAb. Moreover, this novel immunoRNase is endowed with an effective and selective antiproliferative action for ErbB2-positive tumor cells both in vitro and in vivo. Its antitumor activity is more potent than that of the parental Erb-hcAb as the novel immunoconjugate has acquired RNase-based cytotoxicity in addition to the inhibitory growth effects, antibody-dependent and complement-dependent cytotoxicity of the compact antibody.
Erb-hcAb-RNase could be a promising candidate for the immunotherapy of ErbB2-positive tumours as it combines the advantages of the first generation scFv-based immunoRNase with those of a fully functional antibod
Differential expression and MAL-dependent targeting of the L-MAG and S-MAG isoforms to myelin membranes
No full textMany degenerative diseases of the nervous system, including Multiple Sclerosis and peripheral neuropathies, are triggered by an impaired interaction between the axons and their surrounding myelin sheaths. The cause for this disturbed axon-myelin interaction, and the secondary neuronal damage that produces the clinical symptoms, lies in a primary defect of the myelin sheath. The myelin sheath itself is formed and maintained by oligodendrocytes and Schwann cells, the myelinating glial cells of the central and peripheral nervous system, respectively. The isoforms of the myelin-associated glycoprotein (MAG) are thought to be potential key elements of axon-myelin interaction, since these immunoglobulin-like cell signalling proteins are known to be localized in the periaxonal and paranodal myelin membranes. The MAG isoforms each display one of two possible intracellular C-termini as a result of alternative mRNA splicing. The C-terminus of the large isoform (L-MAG) has been shown to mediate downstream signals via the non-receptor tyrosine kinase Fyn, while the Cterminus of the short isoform (S-MAG) is thought to interact with the glial cytoskeleton. We have investigated the regulation and differential expression of L- and S-MAG in oligodendroglial cells and in transgenic mice by the use of genomic constructs that encode individually green fluorescent protein-tagged MAG isoforms. In the oligodendroglial cells LMAG was the dominant isoform prior to the stimulation of cells with cyclicAMP, whereas upon cyclicAMP stimulation, S-MAG was predominantly expressed in cells exhibiting advanced morphological differentiation. The investigation of our transgenic mice revealed that the two MAG isoforms are differentially expressed in distinct fibre tracts of the striatum and that S-MAG seems to be predominantly expressed in the long projecting fibres of the corpus callosum. Thus, the two MAG isoforms appear not only to be differentially expressed during development and in the adult, but they seem to mediate isoform-specific aspects of the axon-myelin interaction in distinct regions of the adult brain. A major question in the formation and maintenance of the myelin-axon interaction concerns the coordinated targeting of myelin signalling molecules and lipids to the different myelin compartments. Recent results suggest that glycolipid-enriched microdomains, socalled 'lipid-rafts', are involved in special sorting and trafficking mechanisms of membrane proteins and lipids. Furthermore, they are thought to serve as platforms for signal transduction processes. This makes them to interesting candidates for axon-myelin interactions, as well as for interactions between the apposed myelin membranes. The integral membrane protein 'Myelin and Lymphocyte Protein' (MAL) is suggested to be involved in lipid-raft-mediated protein targeting and signalling in myelinating cells. Our investigation of adult brain tissue of MAL-deficient mice showed that the incorporation of particular myelin components, such as MAG, into myelin membranes was significantly reduced. Thus, the targeting of L- and S-MAG to the myelin membranes appears to be dependent on the lipid-raft protein MAL. Furthermore, the MAL-deficient mice showed several ultra structural alterations comparable to those of the MAG-deficient mice and that reflect an impaired axon-myelin interaction. Our data supports the idea that-raft mediated trafficking of myelin constituents, such as MAG, to the different myelin compartments is a major task of adult oligodendrocytes in the context of maintaining the axonal contact of the myelin sheath. With the use of the isoform specific tagged MAG expressing mice, it will be possible for the first time, to investigate their differential function in axon-glia interaction as well as their dependence on MAL in vivo
Regulation of circadian behaviour and metabolism by REV-ERB-α and REV-ERB-β
No full textThe circadian clock acts at the genomic level to coordinate internal behavioural and physiological rhythms via the CLOCK-BMAL1 transcriptional heterodimer. Although the nuclear receptors REV-ERB-α and REV-ERB-β have been proposed to form an accessory feedback loop that contributes to clock function, their precise roles and importance remain unresolved. To establish their regulatory potential, we determined the genome-wide cis-acting targets (cistromes) of both REV-ERB isoforms in murine liver, which revealed shared recognition at over 50% of their total DNA binding sites and extensive overlap with the master circadian regulator BMAL1. Although REV-ERB-α has been shown to regulate Bmal1 expression directly, our cistromic analysis reveals a more profound connection between BMAL1 and the REV-ERB-α and REV-ERB-β genomic regulatory circuits than was previously suspected. Genes within the intersection of the BMAL1, REV-ERB-α and REV-ERB-β cistromes are highly enriched for both clock and metabolic functions. As predicted by the cistromic analysis, dual depletion of Rev-erb-α and Rev-erb-β function by creating double-knockout mice profoundly disrupted circadian expression of core circadian clock and lipid homeostatic gene networks. As a result, double-knockout mice show markedly altered circadian wheel-running behaviour and deregulated lipid metabolism. These data now unite REV-ERB-α and REV-ERB-β with PER, CRY and other components of the principal feedback loop that drives circadian expression and indicate a more integral mechanism for the coordination of circadian rhythm and metabolism.LIS
Letter, [Author unclear] to Paulina T. Merritt
No full textHandwritten letter to Paulina Merritt from an unknown author, October 1, 1876.
ERB master archival tape specification no. T 134081 ERB MAT, revision 1
No full textThe Earth radiation budget (ERB)MAT tapes are generated by the ERB MATGEN software using the IBM 3081 computer system operated by the Science and Applications Computer Center at Goddard Space Flight Center. All MAT's are 9-track and MAT data are in ascending time order. The gross tape format for NIMBUS year-1 and year-2 MAT's is different from the format of MAT's starting with year-3. The MATs from the first two years are to contain one day's worth of data while all other MATs are to contain multiple day's worth of data stacked onto the tapes
The Thyroid Hormone Receptor Alpha Locus and White Matter Lesions: A Role for the Clock Gene REV-ERB?
No full textBackground: Thyroid disorders are associated with an increased risk of cognitive impairment and Alzheimer's disease. Both small vessel disease and neurodegeneration have a role in the pathogenesis of cognitive impairment and Alzheimer's disease. Thyroid hormone receptor alpha (TR?) is the predominant TR in brain. The circadian clock gene REV-ERB? overlaps with the TR? gene and interferes with TR? expression. Limited data are available on the role of the TR?/REV-ERB? locus in small vessel disease and neurodegeneration. We therefore studied genetic variation in the TR?/REV-ERB? locus in relation to brain imaging data, as early markers for small vessel disease and neurodegeneration. Methods: Fifteen polymorphisms, covering the TR?/REV-ERB? locus, were studied in relation to white matter lesion (WML), total brain, and hippocampal volumes in the Rotterdam Study I (RS-I, n=454). Associations that remained significant after multiple testing correction were subsequently studied in an independent population for replication (RS-II, n=607). Results: No associations with total brain or hippocampal volumes were detected. A haplotype block in REV-ERB? was associated with WML volumes in RS-I. Absence of this haplotype was associated with larger WML volumes in women (0.38%±0.18% [?±SE], p=0.007), but not in men (0.04%±0.11%, p=0.24), which was replicated in RS-II (women: 0.15%±0.05%, p=0.04; men: 0.05%±0.07%, p=0.80). Meta-analysis of the two populations showed that women lacking this haplotype have a 1.9 times larger WML volume (p=0.001). Conclusion: Our results suggest a role for REV-ERB? in the pathogenesis of WMLs.IST/Imaging Science and TechnologyApplied Science
Bivariate Lagrange interpolation at the node points of non-degenerate Lissajous curves
No full textMotivated by an application in Magnetic Particle Imaging, we study bivariate Lagrange interpolation at the node points of Lissajous curves. The resulting theory is a generalization of the polynomial interpolation theory developed for a node set known as Padua points. With appropriately defined polynomial spaces, we will show that the node points of non-degenerate Lissajous curves allow unique interpolation and can be used for quadrature rules in the bivariate setting. An explicit formula for the Lagrange polynomials allows to compute the interpolating polynomial with a simple algorithmic scheme. Compared to the already established schemes of the Padua and Xu points, the numerical results for the proposed scheme show similar approximation errors and a similar growth of the Lebesgue constant
Lebesgue constants for polyhedral sets and polynomial interpolation on Lissajous–Chebyshev nodes
No full textTo analyze the absolute condition number of multivariate polynomial interpolation on Lissajous–Chebyshev node points, we derive upper and lower bounds for the respective Lebesgue constant. The proof is based on a relation between the Lebesgue constant for the polynomial interpolation problem and the Lebesgue constant linked to the polyhedral partial sums of Fourier series. The magnitude of the obtained bounds is determined by a product of logarithms of the side lengths of the considered polyhedral sets and shows the same behavior as the magnitude of the Lebesgue constant for polynomial interpolation on the tensor product Chebyshev grid
- …
