Low-energy electric dipole response in 120Sn

The electric dipole strength in 120Sn has been extracted from proton inelastic scattering experiments at E_p = 295 MeV and at forward angles including 0 degree. Below neutron threshoild it differs from the results of a 120Sn(gamma,gamma') experiment and peaks at an excitation energy of 8.3 MeV. The total strength corresponds to 2.3(2)% of the energy-weighted sum rule and is more than three times larger than what is observed with the (gamma,gamma') reaction. This implies a strong fragmentation of the E1 strength and/or small ground state branching ratios of the excited 1- states.Comment: 7 pages, 6 figure

Wavelet signatures of KK-splitting of the Isoscalar Giant Quadrupole Resonance in deformed nuclei from high-resolution (p,p′') scattering off 146,148,150^{146,148,150}Nd

The phenomenon of fine structure of the Isoscalar Giant Quadrupole Resonance (ISGQR) has been studied with high energy-resolution proton inelastic scattering at iThemba LABS in the chain of stable even-mass Nd isotopes covering the transition from spherical to deformed ground states. A wavelet analysis of the background-subtracted spectra in the deformed 146,148,150Nd isotopes reveals characteristic scales in correspondence with scales obtained from a Skyrme RPA calculation using the SVmas10 parameterization. A semblance analysis shows that these scales arise from the energy shift between the main fragments of the K = 0, 1 and K = 2 components.Comment: 7 pages, 6 figure

Dipole polarizability of 120Sn and nuclear energy density functionals

The electric dipole strength distribution in 120Sn between 5 and 22 MeV has been determined at RCNP Osaka from a polarization transfer analysis of proton inelastic scattering at E_0 = 295 MeV and forward angles including 0{\deg}. Combined with photoabsorption data an electric dipole polarizability \alpha_D(120Sn) = 8.93(36) fm^3 is extracted. The dipole polarizability as isovector observable par excellence carries direct information on the nuclear symmetry energy and its density dependence. The correlation of the new value with the well established \alpha_D(208Pb) serves as a test of its prediction by nuclear energy density functionals (EDFs). Models based on modern Skyrme interactions describe the data fairly well while most calculations based on relativistic Hamiltonians cannot.Comment: 6 pages, 4 figure

Why Has Human–Carnivore Conflict Not Been Resolved in Namibia?

Human–wildlife conflict has historically been portrayed as a management problem where solutions lie in technical changes or financial incentives. However, recent research shows many conflicts stem from social, economic, and political drivers. We undertook qualitative data collection on livestock farms to determine whether relationships between farmers and their workers affected frequency of reported livestock depredation in Namibia. We found that the conflict was affected by social and economic inequalities embedded in the previous apartheid regime. Macro- and microlevel socioeconomic problems created an environment where livestock depredation was exacerbated by unmotivated farm workers. Poor treatment of workers by farmers resulted in vengeful behaviors, such as livestock theft and wildlife poaching. Successfully addressing this situation therefore requires recognition and understanding of its complexity, rather than reducing it to its most simplistic part

Landscape genomics and biased FST approaches reveal single nucleotide polymorphisms under selection in goat breeds of North-East Mediterranean

<p>Abstract</p> <p>Background</p> <p>In this study we compare outlier loci detected using a <it>F<smcaps>ST </smcaps></it>based method with those identified by a recently described method based on spatial analysis (SAM). We tested a panel of single nucleotide polymorphisms (SNPs) previously genotyped in individuals of goat breeds of southern areas of the Mediterranean basin (Italy, Greece and Albania). We evaluate how the SAM method performs with SNPs, which are increasingly employed due to their high number, low cost and easy of scoring.</p> <p>Results</p> <p>The combined use of the two outlier detection approaches, never tested before using SNP polymorphisms, resulted in the identification of the same three loci involved in milk and meat quality data by using the two methods, while the <it>F<smcaps>ST </smcaps></it>based method identified 3 more loci as under selection sweep in the breeds examined.</p> <p>Conclusion</p> <p>Data appear congruent by using the two methods for <it>F<smcaps>ST </smcaps></it>values exceeding the 99% confidence limits. The methods of <it>F<smcaps>ST </smcaps></it>and SAM can independently detect signatures of selection and therefore can reduce the probability of finding false positives if employed together. The outlier loci identified in this study could indicate adaptive variation in the analysed species, characterized by a large range of climatic conditions in the rearing areas and by a history of intense trade, that implies plasticity in adapting to new environments.</p

The Eps8/IRSp53/VASP Network Differentially Controls Actin Capping and Bundling in Filopodia Formation

There is a body of literature that describes the geometry and the physics of filopodia using either stochastic models or partial differential equations and elasticity and coarse-grained theory. Comparatively, there is a paucity of models focusing on the regulation of the network of proteins that control the formation of different actin structures. Using a combination of in-vivo and in-vitro experiments together with a system of ordinary differential equations, we focused on a small number of well-characterized, interacting molecules involved in actin-dependent filopodia formation: the actin remodeler Eps8, whose capping and bundling activities are a function of its ligands, Abi-1 and IRSp53, respectively; VASP and Capping Protein (CP), which exert antagonistic functions in controlling filament elongation. The model emphasizes the essential role of complexes that contain the membrane deforming protein IRSp53, in the process of filopodia initiation. This model accurately accounted for all observations, including a seemingly paradoxical result whereby genetic removal of Eps8 reduced filopodia in HeLa, but increased them in hippocampal neurons, and generated quantitative predictions, which were experimentally verified. The model further permitted us to explain how filopodia are generated in different cellular contexts, depending on the dynamic interaction established by Eps8, IRSp53 and VASP with actin filaments, thus revealing an unexpected plasticity of the signaling network that governs the multifunctional activities of its components in the formation of filopodia

Rho GTPase Cdc42 Is a Direct Interacting Partner of Adenomatous Polyposis Coli Protein and Can Alter Its Cellular Localization

Adenomatous Polyposis Coli (APC) is a tumor suppressor gene product involved in colon cancer. APC is a large multidomain molecule of 2843 amino acid residues and connects cell-cell adhesion, the F-actin/microtubule cytoskeleton and the nucleus. Here we show that Cdc42 interacts directly with the first three armadillo repeats of APC by yeast two-hybrid screens. We confirm the Cdc42-APC interaction using pulldown assays in vitro and FRET assays in vivo. Interestingly, Cdc42 interacts with APC at leading edge sites where F-actin is enriched. In contrast, Cdc42 interacts with the truncated mutant APC1–1638 in cellular puncta associated with the golgi-lysozome pathway in transfected CHO cells. In HCT116 and SW480 cells, Cdc42 induces the relocalization of endogenous APC and the mutant APC1–1338 to the plasma membrane and cellular puncta, respectively. Taken together, these data indicate that the Cdc42-APC interaction induces localization of both APC and mutant APC and may thus play a direct role in the functions of these proteins

Phosphoinositide-binding interface proteins involved in shaping cell membranes

The mechanism by which cell and cell membrane shapes are created has long been a subject of great interest. Among the phosphoinositide-binding proteins, a group of proteins that can change the shape of membranes, in addition to the phosphoinositide-binding ability, has been found. These proteins, which contain membrane-deforming domains such as the BAR, EFC/F-BAR, and the IMD/I-BAR domains, led to inward-invaginated tubes or outward protrusions of the membrane, resulting in a variety of membrane shapes. Furthermore, these proteins not only bind to phosphoinositide, but also to the N-WASP/WAVE complex and the actin polymerization machinery, which generates a driving force to shape the membranes

A Rac/Cdc42 exchange factor complex promotes formation of lateral filopodia and blood vessel lumen morphogenesis

During angiogenesis, Rho GTPases influence endothelial cell migration and cell-cell adhesion; however it is not known whether they control formation of vessel lumens, which are essential for blood flow. Here, using an organotypic system that recapitulates distinct stages of VEGF-dependent angiogenesis, we show that lumen formation requires early cytoskeletal remodelling and lateral cell-cell contacts, mediated through the RAC1 guanine nucleotide exchange factor (GEF) DOCK4. DOCK4 signalling is necessary for lateral filopodial protrusions and tubule remodelling prior to lumen formation, whereas proximal, tip filopodia persist in the absence of DOCK4. VEGF-dependent Rac activation via DOCK4 is necessary for CDC42 activation to signal filopodia formation and depends on the activation of RHOG through the RHOG GEF, SGEF. VEGF promotes interaction of DOCK4 with the CDC42 GEF DOCK9. These studies identify a novel Rho-family GTPase activation cascade for the formation of endothelial cell filopodial protrusions necessary for tubule remodelling, thereby influencing subsequent stages of lumen morphogenesis

IgA in the horse: cloning of equine polymeric Ig receptor and J chain and characterization of recombinant forms of equine IgA

As in other mammals, immunoglobulin A (IgA) in the horse has a key role in immune defense. To better dissect equine IgA function, we isolated complementary DNA (cDNA) clones for equine J chain and polymeric Ig receptor (pIgR). When coexpressed with equine IgA, equine J chain promoted efficient IgA polymerization. A truncated version of equine pIgR, equivalent to secretory component, bound with nanomolar affinity to recombinant equine and human dimeric IgA but not with monomeric IgA from either species. Searches of the equine genome localized equine J chain and pIgR to chromosomes 3 and 5, respectively, with J chain and pIgR coding sequence distributed across 4 and 11 exons, respectively. Comparisons of transcriptional regulatory sequences suggest that horse and human pIgR expression is controlled through common regulatory mechanisms that are less conserved in rodents. These studies pave the way for full dissection of equine IgA function and open up possibilities for immune-based treatment of equine diseases