The uniquely human capacity to throw evolved from a non-throwing primate: an evolutionary dissociation between action and perception

Humans are uniquely endowed with the ability to engage in accurate, high-momentum throwing. Underlying this ability is a unique morphological adaptation that enables the characteristic rotation of the arm and pelvis. What is unknown is whether the psychological mechanisms that accompany the act of throwing are also uniquely human. Here we explore this problem by asking whether free-ranging rhesus monkeys (Macaca mulatta), which lack both the morphological and neural structures to throw, nonetheless recognize the functional properties of throwing. Rhesus not only understand that human throwing represents a threat, but that some aspects of a throwing event are more relevant than others; specifically, rhesus are sensitive to the kinematics, direction and speed of the rotating arm, the direction of the thrower's eye gaze and the object thrown. These results suggest that the capacity to throw did not coevolve with psychological mechanisms that accompany throwing; rather, this capacity may have built upon pre-existing perceptual processes. These results are consistent with a growing body of work showing that non-human animals often exhibit perceptual competencies that do not show up in their motor responses, suggesting evolutionary dissociations between the systems of perception that provide understanding of the world and those that mediate action on the world.     

Measurement of cell proliferation by heavy water labeling

DNA replication occurs almost exclusively during S-phase of the cell cycle and represents a simple biochemical metric of cell division. Previous methods for measuring cell proliferation rates have important limitations. Here, we describe experimental protocols for measuring cell proliferation and death rates based on the incorporation of deuterium ((2)H) from heavy water ((2)H(2)O) into the deoxyribose moiety of purine deoxyribonucleotides in DNA of dividing cells. Label incorporation is measured by gas chromatography/mass spectrometry. Modifications of the basic protocol permit analysis of small cell samples (down to 2,000 cells). The theoretical basis and operational requirements for effective use of these methods to measure proliferation and death rates of cells in vivo are described. These methods are safe for use in humans, have technical and interpretation advantages over alternative techniques and can be used on small numbers of cells. The protocols enable definitive in vivo studies of the fraction or absolute number of newly divided cells and their subsequent survival kinetics in animals and humans.     

Transparent communication strategy on GMOs: Will it change public opinion?

Innovations are central for the economic growth; however, the use of new technologies needs to be widely accepted in the general public and the society as a whole. Biotechnology in general, and the use of genetic engineering in food production in particular are seen critically by the European public and perceived as "risky", and a transatlantic divide between European and US citizens has been observed. This review investigates the reasons for those differing perceptions and proposes new strategies to communicate the benefits of biotechnology in agriculture to a broader public. When analyzing the dialogue process that has taken place between public, scientists, governmental organizations and industry, questions arise on what has been done differently in Europe, in order to propose new, more successful and efficient communication strategies for the future.     

Vector-dependent gene expression driven by insulated P-element reporter vectors

The Pelican and Stinger series of P-element transformation vectors are a popular choice for reporter gene expression in transgenic flies. We report here as a cautionary note that these vectors on their own can drive reporter gene expression in the larval and pupal salivary gland.     

Données nouvelles sur les mammifères et les nummulites de l'éocène supérieur subalpin (synclinaux du Charbon et d'entrevernes,Bauges, Savoie et Haute-Savoie)

Vertebrate remains and nummulites have been investigated from the Late Eocene—Early Oligocene transgressive sequence of the «Chaînes subalpines south of the lake Annecy. The sedimentary environments range from fluvio-lacustrine shales and conglomerates at the base to hemipelagic Globigerina shales at the top. The fluvio-lacustrine white marls contain mammals of the upper, probably terminal Ludian, with affinities to the assemblage of Saint-Capraise. The brackish Cerithium beds have furnished charophytes of the Bembridge zone. The nummulite limestones are not dated precisely, but isolated, probably redeposited nummulites from the base of the Globigerina shales are of terminal Eocene or basal Oligocene age. The Globigerina shales themselves belong to the Oligocene.     

Twist and writhing in short circular DNAs according to first-order elasticity

The distribution of twist and writhing in a closed DNA shorter than its persistence length is examined. In this case, the only energy contribution is elastic. We have in tegrated the equations of elasticity for a homogeneous axially symmetric rod of undeformable infinitely small circular cross section with frictionless reactions, when there is no or only one self-contact. In the absence of self-contacts, the central line of the rod is drawn on a toroid. It makes ν turns around the axis of revolution of the toroid and m turns around its core. The integer, ν, is equal to one if the rod is unknotted. We prove that no infinitely thin rod with a positive Poisson ratio is stable in a toroidal conformation if there is no self-contact. However, m-leafed roses or rosettes, with but one multiple self-contact, are shown to actually be stable when their writhing is not too great. When the integer, m, is equal to two, we have figure-8 conformations. Buckling of the circle into a figure-8 conformation occurs for the constraint such that the figure-8 and the circular conformations have the same energy. This constraint is 1.845 turns for a bending-to-twisting elastic constants ratio of A/C = 1.5. For the same value of A/C, the figure-8 conformation is unstable for a constraint greater than 2.4 turns. Corrections caused by a finite value of the radius ratio, a/L, of the cross section to the length of the rod, are estimated. For instance, both the circular conformation and the infinitesimally warped circle are simultaneous solutions for particular values of the β twist. β = A/C (m² ? ν²)^½ [1 + (νπa/L)²/2]. The binding of ethidium to DNAs short enough to follow first-order elasticity has been studied. Buckling occurs at an apparent average constraint of about 0.6. How the DNA molecules are distributed in figure-8 conformations and circles has been determined as the ethidium concentration is varied.     

Propagation of Tau Misfolding from the Outside to the Inside of a Cell

Tauopathies are neurodegenerative diseases characterized by aggregation of the microtubule-associated protein Tau in neurons and glia. Although Tau is normally considered an intracellular protein, Tau aggregates are observed in the extracellular space, and Tau peptide is readily detected in the cerebrospinal fluid of patients. Tau aggregation occurs in many diseases, including Alzheimer disease and frontotemporal dementia. Tau pathology begins in discrete, disease-specific regions but eventually involves much larger areas of the brain. It is unknown how this propagation of Tau misfolding occurs. We hypothesize that extracellular Tau aggregates can transmit a misfolded state from the outside to the inside of a cell, similar to prions. Here we show that extracellular Tau aggregates, but not monomer, are taken up by cultured cells. Internalized Tau aggregates displace tubulin, co-localize with dextran, a marker of fluid-phase endocytosis, and induce fibrillization of intracellular full-length Tau. These intracellular fibrils are competent to seed fibril formation of recombinant Tau monomer in vitro. Finally, we observed that newly aggregated intracellular Tau transfers between co-cultured cells. Our data indicate that Tau aggregates can propagate a fibrillar, misfolded state from the outside to the inside of a cell. This may have important implications for understanding how protein misfolding spreads through the brains of tauopathy patients, and it is potentially relevant to myriad neurodegenerative diseases associated with protein misfolding.Tau filament deposition in Alzheimer disease (AD),² frontotemporal dementia (FTD), and other tauopathies correlates closely with cognitive dysfunction and cell death (1). Mutations in the tau gene cause autosomal dominant tauopathy, implicating Tau as the proximal cause (2–4). Specific disease phenotypes are defined by the early sites of pathology. For example, AD is characterized by memory loss that derives from involvement of hippocampal neurons, whereas FTD is characterized by personality changes that result from frontal lobe involvement (5). Pathology ultimately spreads to involve much larger regions of brain. Studies on patients with AD show a progressive, stereotyped spread of Tau deposits from the transentorhinal cortex to the hippocampus, and eventually to most cortical areas (6–8). Others have correlated the distribution of neurofibrillary tangles of Tau in AD brains with trans-synaptic distance from the affected areas (9). A similar spread affecting different subsets of neurons has been observed in other sporadic tauopathies, such as progressive supranuclear palsy (10). It is unknown why Tau misfolding progresses through the brain, whether it is a sequence of cell autonomous processes or whether a toxic factor is involved. Loss of synaptic connections and cell death may expose healthy cells to toxic factors and decrease available neurotrophins (11, 12). Another possibility is that the Tau protein itself serves as the agent of trans-cellular propagation. For example, it has been shown that extracellular Tau is toxic to cultured neuronal cells (13, 14). This is consistent with the observation that immunotherapy against Tau reduces pathology in a mouse model (15).Tau is well known as an intracellular protein that stabilizes microtubule filaments (16); however, it is readily detected in cerebrospinal fluid (17) and as extracellular aggregates, termed “ghost tangles,” in diseased brain. These are comprised predominantly of the microtubule-binding region (MTBR), the functional and pathogenic core of the Tau protein (18). We hypothesize that Tau aggregates present in the extracellular space enter naive cells and induce misfolding of intracellular Tau. We have tested this idea using cellular studies, biochemistry, and atomic force microscopy (AFM).