A Neural Model of Visually Guided Steering, Obstacle Avoidance, and Route Selection

A neural model is developed to explain how humans can approach a goal object on foot while steering around obstacles to avoid collisions in a cluttered environment. The model uses optic flow from a 3D virtual reality environment to determine the position of objects based on motion discontinuities, and computes heading direction, or the direction of self-motion, from global optic flow. The cortical representation of heading interacts with the representations of a goal and obstacles such that the goal acts as an attractor of heading, while obstacles act as repellers. In addition the model maintains fixation on the goal object by generating smooth pursuit eye movements. Eye rotations can distort the optic flow field, complicating heading perception, and the model uses extraretinal signals to correct for this distortion and accurately represent heading. The model explains how motion processing mechanisms in cortical areas MT, MST, and posterior parietal cortex can be used to guide steering. The model quantitatively simulates human psychophysical data about visually-guided steering, obstacle avoidance, and route selection.

Laminar Cortical Dynamics of Visual Form and Motion Interactions During Coherent Object Motion Perception

How do visual form and motion processes cooperate to compute object motion when each process separately is insufficient? Consider, for example, a deer moving behind a bush. Here the partially occluded fragments of motion signals available to an observer must be coherently grouped into the motion of a single object. A 3D FORMOTION model comprises five important functional interactions involving the brain’s form and motion systems that address such situations. Because the model’s stages are analogous to areas of the primate visual system, we refer to the stages by corresponding anatomical names. In one of these functional interactions, 3D boundary representations, in which figures are separated from their backgrounds, are formed in cortical area V2. These depth-selective V2 boundaries select motion signals at the appropriate depths in MT via V2-to-MT signals. In another, motion signals in MT disambiguate locally incomplete or ambiguous boundary signals in V2 via MT-to-V1-to-V2 feedback. The third functional property concerns resolution of the aperture problem along straight moving contours by propagating the influence of unambiguous motion signals generated at contour terminators or corners. Here, sparse “feature tracking signals” from, e.g., line ends, are amplified to overwhelm numerically superior ambiguous motion signals along line segment interiors. In the fourth, a spatially anisotropic motion grouping process takes place across perceptual space via MT-MST feedback to integrate veridical feature-tracking and ambiguous motion signals to determine a global object motion percept. The fifth property uses the MT-MST feedback loop to convey an attentional priming signal from higher brain areas back to V1 and V2. The model's use of mechanisms such as divisive normalization, endstopping, cross-orientation inhibition, and longrange cooperation is described. Simulated data include: the degree of motion coherence of rotating shapes observed through apertures, the coherent vs. element motion percepts separated in depth during the chopsticks illusion, and the rigid vs. non-rigid appearance of rotating ellipses.

Cortical Dynamics of Visual Motion Perception: Short-Range and Long Range Apparent Motion

This article describes further evidence for a new neural network theory of biological motion perception that is called a Motion Boundary Contour System. This theory clarifies why parallel streams Vl-> V2 and Vl-> MT exist for static form and motion form processing among the areas Vl, V2, and MT of visual cortex. The Motion Boundary Contour System consists of several parallel copies, such that each copy is activated by a different range of receptive field sizes. Each copy is further subdivided into two hierarchically organized subsystems: a Motion Oriented Contrast Filter, or MOC Filter, for preprocessing moving images; and a Cooperative-Competitive Feedback Loop, or CC Loop, for generating emergent boundary segmentations of the filtered signals. The present article uses the MOC Filter to explain a variety of classical and recent data about short-range and long-range apparent motion percepts that have not yet been explained by alternative models. These data include split motion; reverse-contrast gamma motion; delta motion; visual inertia; group motion in response to a reverse-contrast Ternus display at short interstimulus intervals; speed-up of motion velocity as interfiash distance increases or flash duration decreases; dependence of the transition from element motion to group motion on stimulus duration and size; various classical dependencies between flash duration, spatial separation, interstimulus interval, and motion threshold known as Korte's Laws; and dependence of motion strength on stimulus orientation and spatial frequency. These results supplement earlier explanations by the model of apparent motion data that other models have not explained; a recent proposed solution of the global aperture problem, including explanations of motion capture and induced motion; an explanation of how parallel cortical systems for static form perception and motion form perception may develop, including a demonstration that these parallel systems are variations on a common cortical design; an explanation of why the geometries of static form and motion form differ, in particular why opposite orientations differ by 90°, whereas opposite directions differ by 180°, and why a cortical stream Vl -> V2 -> MT is needed; and a summary of how the main properties of other motion perception models can be assimilated into different parts of the Motion Boundary Contour System design.

Cortical Dynamics of Visual Motion Perception: Short-Range and Long-Range Apparent Motion

This article describes further evidence for a new neural network theory of biological motion perception. The theory clarifies why parallel streams Vl --> V2, Vl --> MT, and Vl --> V2 --> MT exist for static form and motion form processing among the areas Vl, V2, and MT of visual cortex. The theory suggests that the static form system (Static BCS) generates emergent boundary segmentations whose outputs are insensitive to direction-ofcontrast and insensitive to direction-of-motion, whereas the motion form system (Motion BCS) generates emergent boundary segmentations whose outputs are insensitive to directionof-contrast but sensitive to direction-of-motion. The theory is used to explain classical and recent data about short-range and long-range apparent motion percepts that have not yet been explained by alternative models. These data include beta motion; split motion; gamma motion and reverse-contrast gamma motion; delta motion; visual inertia; the transition from group motion to element motion in response to a Ternus display as the interstimulus interval (ISI) decreases; group motion in response to a reverse-contrast Ternus display even at short ISIs; speed-up of motion velocity as interflash distance increases or flash duration decreases; dependence of the transition from element motion to group motion on stimulus duration and size; various classical dependencies between flash duration, spatial separation, ISI, and motion threshold known as Korte's Laws; dependence of motion strength on stimulus orientation and spatial frequency; short-range and long-range form-color interactions; and binocular interactions of flashes to different eyes.

Akt signal transduction dysfunction in the 3xTg-AD mouse model of Alzheimer's disease

Alzheimer’s disease (AD) is an incurable neurodegenerative disorder, accounting for over 60% of all cases of dementia. The primary risk factor for AD is age, however several genetic and environmental factors are also involved. The pathological characteristics of AD include extracellular deposition of the beta-amyloid peptide (Aβ) and intraneuronal accumulation of neurofibrillary tangles (NFTs) made of aggregated paired helical filaments (PHFs) of the hyperphosphorylated tau protein, along with synaptic loss and neuronal death. There are numerous biochemical mechanisms involved in AD pathogenesis, however the reigning hypothesis points to toxic oligomeric Aβ species as the primary causative factor in a cascade of events leading to neuronal stress and dyshomeostasis that initiate abnormal regulation of tau. The insulin and IGF-1 receptors (IR, IGF-1R) are the primary activators of PI3- K/Akt through which they regulate cell growth, development, glucose metabolism, and learning and memory. Work in our lab and others shows increased Akt activity and phosphorylation of its downstream targets in AD brain, along with insulin and insulin-like growth factor-1 signalling (IIS) dysfunction. This is supported by studies of AD models in vivo and in vitro. Our group and others hypothesise that Aβ activates Akt through IIS to initiate a negative feedback mechanism that desensitises neurons to insulin/IGF-1, and sustains activation of Akt. In this study the functions of endogenous Akt, IR, and the insulin receptor substrate (IRS-1) were examined in relationship to Aβ and tau pathology in the 3xTg-AD mouse model, which contains three mutant human transgenes associated with familial AD or dementia. The 3xTg-AD mouse develops Aβ and tau pathology in a spatiotemporal manner that best recapitulates the progression of AD in human brain. Western blotting and immunofluorescent microscopy techniques were utilised in vivo and in vitro, to examine the relationship between IIS, Akt, and AD pathology. I first characterised in detail AD pathology in 3xTg-AD mice, where an age-related accumulation of intraneuronal Aβ and tau was observed in the hippocampal formation, amygdala, and entorhinal cortex, and at late stages (18 months), extracellular amyloid plaques and NFTs, primarily in the subiculum and the CA1 layer of the hippocampal formation. Increased activity of Akt, detected with antibody to phosphoSer473-Akt, was increased in 3xTg-AD mice compared to age-matched non-transgenic mice (non-Tg), and in direct correlation to the accumulation of Aβ and tau in neuronal somatodendritic compartments. Akt phosphorylates tau at residue Ser214 within a highly specific consensus sequence for Akt phosphorylation, and phosphoSer214-tau strongly decreases microtubule (MT) stabilisation by preventing tau-MT binding. PhosphoSer214-tau increased concomitantly with this in the same age-related and region-specific fashion. Polarisation of tau phosphorylation was observed, where PHF-1 (tauSer396/404) and phosphoSer214-tau both appeared early in 3xTg-AD mice in distinct neuronal compartments: PHF-1 in axons, and phosphoSer214-tau in neuronal soma and dendrites. At 18 months, phosphoSer214-tau strongly colocalised with NFTs positive for the PHF- 1 and AT8 (tauSer202/Thr205) phosphoepitopes. IR was decreased with age in 3xTg-AD brain and in comparison to age-matched non-Tg, and this was specific for brain regions containing Aβ, tau, and hyperactive Akt. IRS-1 was similarly decreased, and both proteins showed altered subcellular distribution. Phosphorylation of IRS-1Ser312 is a strong indicator of IIS dysfunction and insulin resistance, and was increased in 3xTg-AD mice with age and in relation to pathology. Of particular note was our observation that abberant IIS and Akt signalling in 3xTg-AD brain related to Aβ and tau pathology on a gross anatomical level, and specifically localised to the brain regions and circuitry of the perforant path. Finally, I conducted a preliminary study of the effects of synthetic Aβ oligomers on embryonic rat hippocampus neuronal cultures to support these results and those in the literature. Taken together, these novel findings provide evidence for IIS and Akt signal transduction dysfunction as the missing link between Aβ and tau pathogenesis, and contribute to the overall understanding of the biochemical mechanisms of AD.

Fragments bibliques coptes

Identification et réédition de deux ostraca, un papyrus et un parchemin coptes. Les documents portent des textes bibliques. O. Brit. Mus. Copt. II 44 :Ps. 18, 8; 36, 1; 78, 9 (?) et 98, 6. O. Brit. Mus. Copt. II 45 :Ps. 31, 10-11. P. Med. Copto Inv. 246b :Mt 1, 18; 20. P. Med. Copto Inv. 71.41c :Lc 1, 64-65; 68-69.

Organizing women as women: Hybridity and grassroots collective action in the 21st century

The Million Mom March (favoring gun control) and Code Pink: Women for Peace (focusing on foreign policy, especially the war in Iraq) are organizations that have mobilized women as women in an era when other women's groups struggled to maintain critical mass and turned away from non-gender-specific public issues. This article addresses how these organizations fostered collective consciousness among women, a large and diverse group, while confronting the echoes of backlash against previous mobilization efforts by women. We argue that the March and Code Pink achieved mobilization success by creating hybrid organizations that blended elements of three major collective action frames: maternalism, egalitarianism, and feminine expression. These innovative organizations invented hybrid forms that cut across movements, constituencies, and political institutions. Using surveys, interviews, and content analysis of organizational documents, this article explains how the March and Code Pink met the contemporary challenges facing women's collective action in similar yet distinct ways. It highlights the role of feminine expression and concerns about the intersectional marginalization of women in resolving the historic tensions between maternalism and egalitarianism. It demonstrates hybridity as a useful analytical lens to understand gendered organizing and other forms of grassroots collective action. © 2010 American Political Science Association.

Simultaneous two-wavelength transmission quantitative phase microscopy with a color camera.

We present a quantitative phase microscopy method that uses a Bayer mosaic color camera to simultaneously acquire off-axis interferograms in transmission mode at two distinct wavelengths. Wrapped phase information is processed using a two-wavelength algorithm to extend the range of the optical path delay measurements that can be detected using a single temporal acquisition. We experimentally demonstrate this technique by acquiring the phase profiles of optically clear microstructures without 2pi ambiguities. In addition, the phase noise contribution arising from spectral channel crosstalk on the color camera is quantified.

Individuals with mutations in XPNPEP3, which encodes a mitochondrial protein, develop a nephronophthisis-like nephropathy.

The autosomal recessive kidney disease nephronophthisis (NPHP) constitutes the most frequent genetic cause of terminal renal failure in the first 3 decades of life. Ten causative genes (NPHP1-NPHP9 and NPHP11), whose products localize to the primary cilia-centrosome complex, support the unifying concept that cystic kidney diseases are "ciliopathies". Using genome-wide homozygosity mapping, we report here what we believe to be a new locus (NPHP-like 1 [NPHPL1]) for an NPHP-like nephropathy. In 2 families with an NPHP-like phenotype, we detected homozygous frameshift and splice-site mutations, respectively, in the X-prolyl aminopeptidase 3 (XPNPEP3) gene. In contrast to all known NPHP proteins, XPNPEP3 localizes to mitochondria of renal cells. However, in vivo analyses also revealed a likely cilia-related function; suppression of zebrafish xpnpep3 phenocopied the developmental phenotypes of ciliopathy morphants, and this effect was rescued by human XPNPEP3 that was devoid of a mitochondrial localization signal. Consistent with a role for XPNPEP3 in ciliary function, several ciliary cystogenic proteins were found to be XPNPEP3 substrates, for which resistance to N-terminal proline cleavage resulted in attenuated protein function in vivo in zebrafish. Our data highlight an emerging link between mitochondria and ciliary dysfunction, and suggest that further understanding the enzymatic activity and substrates of XPNPEP3 will illuminate novel cystogenic pathways.

The dopamine metabolite 3-methoxytyramine is a neuromodulator.

Dopamine (3-hydroxytyramine) is a well-known catecholamine neurotransmitter involved in multiple physiological functions including movement control. Here we report that the major extracellular metabolite of dopamine, 3-methoxytyramine (3-MT), can induce behavioral effects in a dopamine-independent manner and these effects are partially mediated by the trace amine associated receptor 1 (TAAR1). Unbiased in vivo screening of putative trace amine receptor ligands for potential effects on the movement control revealed that 3-MT infused in the brain is able to induce a complex set of abnormal involuntary movements in mice acutely depleted of dopamine. In normal mice, the central administration of 3-MT caused a temporary mild hyperactivity with a concomitant set of abnormal movements. Furthermore, 3-MT induced significant ERK and CREB phosphorylation in the mouse striatum, signaling events generally related to PKA-mediated cAMP accumulation. In mice lacking TAAR1, both behavioral and signaling effects of 3-MT were partially attenuated, consistent with the ability of 3-MT to activate TAAR1 receptors and cause cAMP accumulation as well as ERK and CREB phosphorylation in cellular assays. Thus, 3-MT is not just an inactive metabolite of DA, but a novel neuromodulator that in certain situations may be involved in movement control. Further characterization of the physiological functions mediated by 3-MT may advance understanding of the pathophysiology and pharmacology of brain disorders involving abnormal dopaminergic transmission, such as Parkinson's disease, dyskinesia and schizophrenia.

Trafficking of G protein-coupled receptors.

G protein-coupled receptors (GPCRs) play an integral role in the signal transduction of an enormous array of biological phenomena, thereby serving to modulate at a molecular level almost all components of human biology. This role is nowhere more evident than in cardiovascular biology, where GPCRs regulate such core measures of cardiovascular function as heart rate, contractility, and vascular tone. GPCR/ligand interaction initiates signal transduction cascades, and requires the presence of the receptor at the plasma membrane. Plasma membrane localization is in turn a function of the delivery of a receptor to and removal from the cell surface, a concept defined most broadly as receptor trafficking. This review illuminates our current view of GPCR trafficking, particularly within the cardiovascular system, as well as highlights the recent and provocative finding that components of the GPCR trafficking machinery can facilitate GPCR signaling independent of G protein activation.

Experimental evaluation of evolution and coevolution as agents of ecosystem change in Trinidadian streams.

Evolution has been shown to be a critical determinant of ecological processes in some systems, but its importance relative to traditional ecological effects is not well known. In addition, almost nothing is known about the role of coevolution in shaping ecosystem function. Here, we experimentally evaluated the relative effects of species invasion (a traditional ecological effect), evolution and coevolution on ecosystem processes in Trinidadian streams. We manipulated the presence and population-of-origin of two common fish species, the guppy (Poecilia reticulata) and the killifish (Rivulus hartii). We measured epilithic algal biomass and accrual, aquatic invertebrate biomass, and detrital decomposition. Our results show that, for some ecosystem responses, the effects of evolution and coevolution were larger than the effects of species invasion. Guppy evolution in response to alternative predation regimes significantly influenced algal biomass and accrual rates. Guppies from a high-predation site caused an increase in algae relative to guppies from a low-predation site; algae effects were probably shaped by observed divergence in rates of nutrient excretion and algae consumption. Rivulus-guppy coevolution significantly influenced the biomass of aquatic invertebrates. Locally coevolved populations reduced invertebrate biomass relative to non-coevolved populations. These results challenge the general assumption that intraspecific diversity is a less critical determinant of ecosystem function than is interspecific diversity. Given existing evidence for contemporary evolution in these fish species, our findings suggest considerable potential for eco-evolutionary feedbacks to operate as populations adapt to natural or anthropogenic perturbations.

Eco-evolutionary trophic dynamics: loss of top predators drives trophic evolution and ecology of prey.

Ecosystems are being altered on a global scale by the extirpation of top predators. The ecological effects of predator removal have been investigated widely; however, predator removal can also change natural selection acting on prey, resulting in contemporary evolution. Here we tested the role of predator removal on the contemporary evolution of trophic traits in prey. We utilized a historical introduction experiment where Trinidadian guppies (Poecilia reticulata) were relocated from a site with predatory fishes to a site lacking predators. To assess the trophic consequences of predator release, we linked individual morphology (cranial, jaw, and body) to foraging performance. Our results show that predator release caused an increase in guppy density and a "sharpening" of guppy trophic traits, which enhanced food consumption rates. Predator release appears to have shifted natural selection away from predator escape ability and towards resource acquisition ability. Related diet and mesocosm studies suggest that this shift enhances the impact of guppies on lower trophic levels in a fashion nuanced by the omnivorous feeding ecology of the species. We conclude that extirpation of top predators may commonly select for enhanced feeding performance in prey, with important cascading consequences for communities and ecosystems.

The impact of geologic variability on capacity and cost estimates for storing CO 2 in deep-saline aquifers

While numerous studies find that deep-saline sandstone aquifers in the United States could store many decades worth of the nation's current annual CO 2 emissions, the likely cost of this storage (i.e. the cost of storage only and not capture and transport costs) has been harder to constrain. We use publicly available data of key reservoir properties to produce geo-referenced rasters of estimated storage capacity and cost for regions within 15 deep-saline sandstone aquifers in the United States. The rasters reveal the reservoir quality of these aquifers to be so variable that the cost estimates for storage span three orders of magnitude and average>$100/tonne CO 2. However, when the cost and corresponding capacity estimates in the rasters are assembled into a marginal abatement cost curve (MACC), we find that ~75% of the estimated storage capacity could be available for<$2/tonne. Furthermore, ~80% of the total estimated storage capacity in the rasters is concentrated within just two of the aquifers-the Frio Formation along the Texas Gulf Coast, and the Mt. Simon Formation in the Michigan Basin, which together make up only ~20% of the areas analyzed. While our assessment is not comprehensive, the results suggest there should be an abundance of low-cost storage for CO 2 in deep-saline aquifers, but a majority of this storage is likely to be concentrated within specific regions of a smaller number of these aquifers. © 2011 Elsevier B.V.