Seeing motion and apparent motion

In apparent motion experiments, participants are presented with what is in fact a succession of two brief stationary stimuli at two different locations, but they report an impression of movement. Philosophers have recently debated whether apparent motion provides evidence in favour of a particular account of the nature of temporal experience. I argue that the existing discussion in this area is premised on a mistaken view of the phenomenology of apparent motion and, as a result, the space of possible philosophical positions has not yet been fully explored. In particular, I argue that the existence of apparent motion is compatible with an account of the nature of temporal experience that involves a version of direct realism. In doing so, I also argue against two other claims often made about apparent motion, viz. that apparent motion is the psychological phenomenon that underlies motion experience in the cinema, and that apparent motion is subjectively indistinguishable from real motion

Precision medicine for suicidality: from universality to subtypes and personalization

Suicide remains a clear, present and increasing public health problem, despite being a potentially preventable tragedy. Its incidence is particularly high in people with overt or un(der)diagnosed psychiatric disorders. Objective and precise identification of individuals at risk, ways of monitoring response to treatments and novel preventive therapeutics need to be discovered, employed and widely deployed. We sought to investigate whether blood gene expression biomarkers for suicide (that is, a ‘liquid biopsy’ approach) can be identified that are more universal in nature, working across psychiatric diagnoses and genders, using larger cohorts than in previous studies. Such markers may reflect and/or be a proxy for the core biology of suicide. We were successful in this endeavor, using a comprehensive stepwise approach, leading to a wealth of findings. Steps 1, 2 and 3 were discovery, prioritization and validation for tracking suicidality, resulting in a Top Dozen list of candidate biomarkers comprising the top biomarkers from each step, as well as a larger list of 148 candidate biomarkers that survived Bonferroni correction in the validation step. Step 4 was testing the Top Dozen list and Bonferroni biomarker list for predictive ability for suicidal ideation (SI) and for future hospitalizations for suicidality in independent cohorts, leading to the identification of completely novel predictive biomarkers (such as CLN5 and AK2), as well as reinforcement of ours and others previous findings in the field (such as SLC4A4 and SKA2). Additionally, we examined whether subtypes of suicidality can be identified based on mental state at the time of high SI and identified four potential subtypes: high anxiety, low mood, combined and non-affective (psychotic). Such subtypes may delineate groups of individuals that are more homogenous in terms of suicidality biology and behavior. We also studied a more personalized approach, by psychiatric diagnosis and gender, with a focus on bipolar males, the highest risk group. Such a personalized approach may be more sensitive to gender differences and to the impact of psychiatric co-morbidities and medications. We compared testing the universal biomarkers in everybody versus testing by subtypes versus personalized by gender and diagnosis, and show that the subtype and personalized approaches permit enhanced precision of predictions for different universal biomarkers. In particular, LHFP appears to be a strong predictor for suicidality in males with depression. We also directly examined whether biomarkers discovered using male bipolars only are better predictors in a male bipolar independent cohort than universal biomarkers and show evidence for a possible advantage of personalization. We identified completely novel biomarkers (such as SPTBN1 and C7orf73), and reinforced previously known biomarkers (such as PTEN and SAT1). For diagnostic ability testing purposes, we also examined as predictors phenotypic measures as apps (for suicide risk (CFI-S, Convergent Functional Information for Suicidality) and for anxiety and mood (SASS, Simplified Affective State Scale)) by themselves, as well as in combination with the top biomarkers (the combination being our a priori primary endpoint), to provide context and enhance precision of predictions. We obtained area under the curves of 90% for SI and 77% for future hospitalizations in independent cohorts. Step 5 was to look for mechanistic understanding, starting with examining evidence for the Top Dozen and Bonferroni biomarkers for involvement in other psychiatric and non-psychiatric disorders, as a mechanism for biological predisposition and vulnerability. The biomarkers we identified also provide a window towards understanding the biology of suicide, implicating biological pathways related to neurogenesis, programmed cell death and insulin signaling from the universal biomarkers, as well as mTOR signaling from the male bipolar biomarkers. In particular, HTR2A increase coupled with ARRB1 and GSK3B decreases in expression in suicidality may provide a synergistic mechanistical corrective target, as do SLC4A4 increase coupled with AHCYL1 and AHCYL2 decrease. Step 6 was to move beyond diagnostics and mechanistical risk assessment, towards providing a foundation for personalized therapeutics. Items scored positive in the CFI-S and subtypes identified by SASS in different individuals provide targets for personalized (psycho)therapy. Some individual biomarkers are targets of existing drugs used to treat mood disorders and suicidality (lithium, clozapine and omega-3 fatty acids), providing a means toward pharmacogenomics stratification of patients and monitoring of response to treatment. Such biomarkers merit evaluation in clinical trials. Bioinformatics drug repurposing analyses with the gene expression biosignatures of the Top Dozen and Bonferroni-validated universal biomarkers identified novel potential therapeutics for suicidality, such as ebselen (a lithium mimetic), piracetam (a nootropic), chlorogenic acid (a polyphenol) and metformin (an antidiabetic and possible longevity promoting drug). Finally, based on the totality of our data and of the evidence in the field to date, a convergent functional evidence score prioritizing biomarkers that have all around evidence (track suicidality, predict it, are reflective of biological predisposition and are potential drug targets) brought to the fore APOE and IL6 from among the universal biomarkers, suggesting an inflammatory/accelerated aging component that may be a targetable common denominator

The description of F2 at small x incorporating angular ordering

We study the perturbative QCD description of the HERA measurements of $F_2 (x, Q^2)$ using a gluon distribution that is obtained from an evolution incorporating angular ordering of the gluon emissions, and which embodies both GLAP and BFKL dynamics. We compare the predictions with recent HERA data for $F_2$. We present estimates of the charm component $F_2^c (x, Q^2)$ and of $F_L (x, Q^2)$.Comment: 8 LaTeX pages + 4 uuencoded figure

Reggeon and pion contributions in semi-exclusive diffractive processes at HERA

A detailed analysis of semi-exclusive diffractive processes in e-p DIS at HERA, with the diffractive final states in the forward direction is presented. The contributions of the subleading f_2, \omega, a_2, \rho reggeons and the pion exchanges to the diffractive structure function with the forward proton or neutron are estimated. It is found that the (a_2,\rho) reggeons are entirely responsible for the forward neutron production at x_P < 10^{-3}. The \pi N production in the forward region is estimated using the Deck mechanism. The significance of this reaction for the processes measured at HERA, especially with the leading neutron, is discussed.Comment: Strongly revised version accepted for publication in Phys.Rev.D. Latex, 14 pages with 5 eps figures include

Do we (seem to) perceive passage?

I examine some recent claims put forward by L. A. Paul, Barry Dainton and Simon Prosser, to the effect that perceptual experiences of movement and change involve an (apparent) experience of ‘passage’, in the sense at issue in debates about the metaphysics of time. Paul, Dainton and Prosser all argue that this supposed feature of perceptual experience – call it a phenomenology of passage – is illusory, thereby defending the view that there is no such a thing as passage, conceived of as a feature of mind-independent reality. I suggest that in fact there is no such phenomenology of passage in the first place. There is, however, a specific structural aspect of the phenomenology of perceptual experiences of movement and change that can explain how one might mistakenly come to the belief that such experiences do involve a phenomenology of passage

Inconsistent boundaries

Research on this paper was supported by a grant from the Marsden Fund, Royal Society of New Zealand.Mereotopology is a theory of connected parts. The existence of boundaries, as parts of everyday objects, is basic to any such theory; but in classical mereotopology, there is a problem: if boundaries exist, then either distinct entities cannot be in contact, or else space is not topologically connected (Varzi in Noûs 31:26–58, 1997). In this paper we urge that this problem can be met with a paraconsistent mereotopology, and sketch the details of one such approach. The resulting theory focuses attention on the role of empty parts, in delivering a balanced and bounded metaphysics of naive space.PostprintPeer reviewe

Prospects for K+→π+ννˉK^+ \to \pi^+ \nu \bar{ \nu } at CERN in NA62

The NA62 experiment will begin taking data in 2015. Its primary purpose is a 10% measurement of the branching ratio of the ultrarare kaon decay $K^+ \to \pi^+ \nu \bar{ \nu }$, using the decay in flight of kaons in an unseparated beam with momentum 75 GeV/c.The detector and analysis technique are described here.Comment: 8 pages for proceedings of 50 Years of CP