Perceptual coding for 3D reconstruction

A primary issue in 3D reconstruction is the realtime efficacy of different coding methods for the multiple decisions among competing 3D solutions. A common model framework making such coding decisions is the boundary limited drift-diffusion model, which has been developed in parallel in various branches of science from quantum physics to economics. A common property of all such models is the linear increase in variance of the diffusion processes over time, implying an inability to focus on the current information in the environment, and the inevitability of a forced random decision in the absence of any reliable evidence. We have developed an alternative, more plausible model framework for Bayesian information accumulation that solves both problems and provides an accurate account of many features of context effects in human 3D reconstruction performance. © 2011 IEEE

A proposed role for all-trans retinal in regulation of rhodopsin regeneration in human rods

AbstractIn order to account for the multi-phasic dynamics of photopigment regeneration in human rods, we developed a new model of the retinoid cycle. We first examined the relative roles of the classical and channeling mechanisms of metarhodopsin decay in establishing these dynamics. We showed that neither of these mechanisms alone, nor a linear combination of the two, can adequately account for the dynamics of rhodopsin regeneration at all bleach levels. Our new model adds novel inhibitory interactions in the cycle of regeneration of rhodopsin that are consistent with the 3D structure of rhodopsin. Our analyses show that the dynamics of human rod photopigment regeneration can be accounted for by end-product regulation of the channeling mechanism where all-trans retinal (tral) inhibits the binding of 11-cis retinal to the opsin.tral complex

Tuning properties of radial phantom motion aftereffects

AbstractMotion aftereffects are normally tested in regions of the visual field that have been directly exposed to motion (local or concrete MAEs). We compared concrete MAEs with remote or phantom MAEs, in which motion is perceived in regions not previously adapted to motion. Our aim was to study the spatial dependencies and spatiotemporal tuning of phantom MAEs generated by radially expanding stimuli. For concrete and phantom MAEs, peripheral stimuli generated stronger aftereffects than central stimuli. Concrete MAEs display temporal frequency tuning, while phantom MAEs do not show categorical temporal frequency or velocity tuning. We found that subjects may use different response strategies to determine motion direction when presented with different stimulus sizes. In some subjects, as adapting stimulus size increased, phantom MAE strength increased while the concrete MAE strength decreased; in other subjects, the opposite effects were observed. We hypothesise that these opposing findings reflect interplay between the adaptation of global motion sensors and local motion sensors with inhibitory interconnections

Multiple Steps of Phosphorylation of Activated Rhodopsin Can Account for the Reproducibility of Vertebrate Rod Single-photon Responses

Single-photon responses (SPRs) in vertebrate rods are considerably less variable than expected if isomerized rhodopsin (R*) inactivated in a single, memoryless step, and no other variability-reducing mechanisms were available. We present a new stochastic model, the core of which is the successive ratcheting down of R* activity, and a concomitant increase in the probability of quenching of R* by arrestin (Arr), with each phosphorylation of R* (Gibson, S.K., J.H. Parkes, and P.A. Liebman. 2000. Biochemistry. 39:5738–5749.). We evaluated the model by means of Monte-Carlo simulations of dim-flash responses, and compared the response statistics derived from them with those obtained from empirical dim-flash data (Whitlock, G.G., and T.D. Lamb. 1999. Neuron. 23:337–351.). The model accounts for four quantitative measures of SPR reproducibility. It also reproduces qualitative features of rod responses obtained with altered nucleotide levels, and thus contradicts the conclusion that such responses imply that phosphorylation cannot dominate R* inactivation (Rieke, F., and D.A. Baylor. 1998a. Biophys. J. 75:1836–1857; Field, G.D., and F. Rieke. 2002. Neuron. 35:733–747.). Moreover, the model is able to reproduce the salient qualitative features of SPRs obtained from mouse rods that had been genetically modified with specific pathways of R* inactivation or Ca(2+) feedback disabled. We present a theoretical analysis showing that the variability of the area under the SPR estimates the variability of integrated R* activity, and can provide a valid gauge of the number of R* inactivation steps. We show that there is a heretofore unappreciated tradeoff between variability of SPR amplitude and SPR duration that depends critically on the kinetics of inactivation of R* relative to the net kinetics of the downstream reactions in the cascade. Because of this dependence, neither the variability of SPR amplitude nor duration provides a reliable estimate of the underlying variability of integrated R* activity, and cannot be used to estimate the minimum number of R* inactivation steps. We conclude that multiple phosphorylation-dependent decrements in R* activity (with Arr-quench) can confer the observed reproducibility of rod SPRs; there is no compelling need to invoke a long series of non-phosphorylation dependent state changes in R* (as in Rieke, F., and D.A. Baylor. 1998a. Biophys. J. 75:1836–1857; Field, G.D., and F. Rieke. 2002. Neuron. 35:733–747.). Our analyses, plus data and modeling of others (Rieke, F., and D.A. Baylor. 1998a. Biophys. J. 75:1836–1857; Field, G.D., and F. Rieke. 2002. Neuron. 35:733–747.), also argue strongly against either feedback (including Ca(2+)-feedback) or depletion of any molecular species downstream to R* as the dominant cause of SPR reproducibility

Analysis of human vergence dynamics

Disparity vergence is commonly viewed as being controlled by at least two mechanisms, an open-loop vergence-specific burst mechanism analogous to the ballistic drive of saccades, and a closed-loop feedback mechanism controlled by the disparity error. We show that human vergence dynamics for disparity jumps of a large textured field have a typical time course consistent with predominant control by the open-loop vergence-specific burst mechanism, although various subgroups of the population show radically different vergence behaviors. Some individuals show markedly slow divergence responses, others slow convergence responses, others slow responses in both vergence directions, implying that the two vergence directions have separate control mechanisms. The faster time courses usually had time-symmetric velocity waveforms implying open-loop burst control, while the slow response usually had time-asymmetric velocity waveforms implying closed-loop feedback control. A further type of behavior in a distinct subpopulation is a compound anomalous divergence response consisting of an initial convergence movement followed by a large corrective divergence movement with time courses implying closed-loop feedback control. The closed-loop response for slow responses to disparity steps exhibited pronounced oscillations in the velocity trace, implying the involvement of a sampled-data system with a rate of about 3 samples/s. This analysis of the variety of human vergence responses thus contributes substantially to the understanding of the oculomotor control mechanisms underlying the generation of vergence movements

Host circadian rhythms are disrupted during malaria infection in parasite genotype-specific manners

Infection can dramatically alter behavioural and physiological traits as hosts become sick and subsequently return to health. Such “sickness behaviours” include disrupted circadian rhythms in both locomotor activity and body temperature. Host sickness behaviours vary in pathogen species-specific manners but the influence of pathogen intraspecific variation is rarely studied. We examine how infection with the murine malaria parasite, Plasmodium chabaudi, shapes sickness in terms of parasite genotype-specific effects on host circadian rhythms. We reveal that circadian rhythms in host locomotor activity patterns and body temperature become differentially disrupted and in parasite genotype-specific manners. Locomotor activity and body temperature in combination provide more sensitive measures of health than commonly used virulence metrics for malaria (e.g. anaemia). Moreover, patterns of host disruption cannot be explained simply by variation in replication rate across parasite genotypes or the severity of anaemia each parasite genotype causes. It is well known that disruption to circadian rhythms is associated with non-infectious diseases, including cancer, type 2 diabetes, and obesity. Our results reveal that disruption of host circadian rhythms is a genetically variable virulence trait of pathogens with implications for host health and disease tolerance

Acute Encephalopathy Associated with Influenza A Infection in Adults

We report acute encephalopathy associated with influenza A infection in 3 adults. We detected high cerebrospinal fluid (CSF) and plasma concentrations of CXCL8/IL-8 and CCL2/MCP-1 (CSF/plasma ratios >3), and interleukin-6, CXCL10/IP-10, but no evidence of viral neuroinvasion. Patients recovered without sequelae. Hyperactivated cytokine response may play a role in pathogenesis

EDN1 Lys198Asn is Associated with Diabetic Retinopathy in Type 2 Diabetes

Purpose: We tested the hypothesis that genetic variants in vasoactive and angiogenic factors regulating the retina vasculature contribute to the development of diabetic retinopathy (DR). Methods: A case-control study was performed to study the genetic association between DR and polymorphic variants of EDN1 (Lys198Asn), LTA (IVS1–80C>A, IVS1–206G>C, IVS1–252>G), eNOS (Glu298Asp), and ITGA2 (BgI II) in a Chinese population with type 2 diabetes mellitus. A well defined population with type 2 diabetes, consisting of 127 controls and 216 DR patients, was recruited. Results: A higher frequency of the Asn/Asn genotype of EDN1 was found in individuals with at least 10 years of diabetes and no retinopathy (controls) compared with DR patients with any duration of diabetes (DR: 2.3%; control: 11.0%; p=0.0002). The Asn allele was also more frequent in controls than DR patients (DR: 16.4%; control: 29.5%; p=0.007). Multiple logistic regression analysis showed that the Asn/Asn genotype was the factor most significantly associated with reduced risk of DR (odds ratio=0.19; 95% CI: 0.07-0.53; p=0.002) and with late onset of diabetes (Asn/Asn: 59 years; Lys/Lys + Lys/Asn: 53 years; p=0.02). Moreover, the Lys/Lys genotype was more common among patients with nonproliferative (75.7%) than proliferative DR (56.9%; p=0.008). The distributions of Lys198Asn alleles in hypertension did not differ from normotensive subjects. No associations between DR and polymorphisms of LTA, eNOS, or ITGA2 were detected, and there were no detectable gene-gene or gene-environmental interactions among the polymorphisms.Conclusions The Asn/Asn genotype of EDN1 was associated with a reduced risk of DR and with delayed onset of type 2 diabetes