Adaptation may cause some of the face caricature effect

One of the ways to demonstrate a caricature preference is to ask participants to adjust a face image over a range from anti-caricature to caricature until it shows the best likeness to a specific individual. Since facial adaptation, whereby exposure to a face influences subsequent perception of faces, is rapid, it is possible that adaptation promotes the selection of a caricatured image. We tested whether giving participants a reference average face image, to counteract any adaptation, would reduce the degree of caricature selected for famous faces. Results confirmed a significant decrease, but even without an average, participants chose an anti-caricatured image. These data suggest a role for adaptation in generating caricature preferences while also suggesting such preferences are not inevitable

The organization of conspecific face space in nonhuman primates

Humans and chimpanzees demonstrate numerous cognitive specializations for processing faces, but comparative studies with monkeys suggest that these may be the result of recent evolutionary adaptations. The present study utilized the novel approach of face space, a powerful theoretical framework used to understand the representation of face identity in humans, to further explore species differences in face processing. According to the theory, faces are represented by vectors in a multidimensional space, the centre of which is defined by an average face. Each dimension codes features important for describing a face's identity, and vector length codes the feature's distinctiveness. Chimpanzees and rhesus monkeys discriminated male and female conspecifics' faces, rated by humans for their distinctiveness, using a computerized task. Multidimensional scaling analyses showed that the organization of face space was similar between humans and chimpanzees. Distinctive faces had the longest vectors and were the easiest for chimpanzees to discriminate. In contrast, distinctiveness did not correlate with the performance of rhesus monkeys. The feature dimensions for each species' face space were visualized and described using morphing techniques. These results confirm species differences in the perceptual representation of conspecific faces, which are discussed within an evolutionary framework

Smad and p38 MAP kinase-mediated signaling of proteoglycan synthesis in vascular smooth muscle

Atherosclerosis is the underlying pathological process of most cardiovascular disease. A critical component of the "response to retention" hypothesis of atherogenesis is proteoglycan/low density lipoprotein (LDL) binding. Transforming growth factor β (TGF-β) is present in atherosclerotic lesions, regulates vascular smooth muscle cell (VSMC) proteoglycan synthesis via an unknown signaling pathway, and increases proteoglycan/LDL binding. This pathway was investigated using the activin receptor-like kinase 5 (ALK5) inhibitor SB431542 and inhibitors of p38 MAP kinase as a possible downstream or alternative mediator. TGF-β stimulated and SB431542 inhibited the phosphorylation of Smad2/3. In human VSMC, TGF-β increased [ 35S]sulfate incorporation into proteoglycans associated with a 19% increase in glycosaminoglycan (GAG) chain size by size exclusion chromatography. SB431542 caused a concentration-dependent decrease in TGF-β-mediated [ 35S]sulfate incorporation with 92% inhibition at 3 μM. Two different p38 MAP kinase inhibitors, SB203580 and SB202190, but not the inactive analogue SB202474, concentration dependently blocked TGF-β-mediated [ 35S]sulfate incorporation. TGF-β increased [ 3H]glucosamine incorporation into glycosaminoglycans by 180% and [ 35S]Met/Cys incorporation into proteoglycan core proteins by 35% with both effects completely inhibited by SB431542. Blocking both Smad2/3 and p38 MAP kinase pathways prevented the effect of TGF-β to increase proteoglycan to LDL binding. TGF-β mediates its effects on proteoglycan synthesis in VSMCs via the ALK5/Smad2/3 phosphorylation pathway as well as via the p38 MAP kinase signaling cascade. Further studies of downstream pathways controlling proteoglycan synthesis may identify potential therapeutic targets for the prevention of atherosclerosis and cardiovascular disease

Learning Online Smooth Predictors for Realtime Camera Planning using Recurrent Decision Trees

We study the problem of online prediction for realtime camera planning, where the goal is to predict smooth trajectories that correctly track and frame objects of interest (e.g., players in a basketball game). The conventional approach for training predictors does not directly consider temporal consistency, and often produces undesirable jitter. Although post-hoc smoothing (e.g., via a Kalman filter) can mitigate this issue to some degree, it is not ideal due to overly stringent modeling assumptions (e.g., Gaussian noise). We propose a recurrent decision tree framework that can directly incorporate temporal consistency into a data-driven predictor, as well as a learning algorithm that can efficiently learn such temporally smooth models. Our approach does not require any post-processing, making online smooth predictions much easier to generate when the noise model is unknown. We apply our approach to sports broadcasting: given noisy player detections, we learn where the camera should look based on human demonstrations. Our experiments exhibit significant improvements over conventional baselines and showcase the practicality of our approach

Thrombin-mediated proteoglycan synthesis utilizes both protein-tyrosine kinase and serine/threonine kinase receptor transactivation in vascular smooth muscle cells

Background: GPCR transactivation of PTKRs and TGF-αRs mediates proteoglycan synthesis in human VSMC. Results: Transactivation of TGF-αRs is integrin-dependent, and inhibition of both transactivation pathways blocks proteoglycan synthesis. Conclusion: GPCR utilize transactivation pathways and not classical signaling in proteoglycan synthesis. Significance: GPCR transactivation of receptor kinase pathways may be broader and more significant than previously recognized

Adaptation to Antifaces and the Perception of Correct Famous Identity in an Average Face

Previous experiments have examined exposure to anti-identities (faces that possess traits opposite to an identity through a population average), finding that exposure to antifaces enhances recognition of the plus-identity images. Here we examine adaptation to antifaces using famous female celebrities. We demonstrate: that exposure to a color and shape transformed antiface of a celebrity increases the likelihood of perceiving the identity from which the antiface was manufactured in a composite face and that the effect shows size invariance (experiment 1), equivalent effects are seen in internet and laboratory-based studies (experiment 2), adaptation to shape-only antifaces has stronger effects on identity recognition than adaptation to color-only antifaces (experiment 3), and exposure to male versions of the antifaces does not influence the perception of female faces (experiment 4). Across these studies we found an effect of order where aftereffects were more pronounced in early than later trials. Overall, our studies delineate several aspects of identity aftereffects and support the proposal that identity is coded relative to other faces with special reference to a relatively sex-specific mean face representation

Biosynthesis of Natural and Hyperelongated Chondroitin Sulfate Glycosaminoglycans: New Insights into an Elusive Process

Proteoglycans are important components of the extracellular matrix of all tissues. Proteoglycans are comprised of a core protein and one or more covalently attached glycosaminoglycan (GAG) chains. The major chondroitin sulfate (CS) and dermatan sulfate (DS) proteoglycans are aggrecan, versican, biglycan and decorin. Cells synthesize GAGs of natural or basal lengths and the GAG chains are subject to considerable growth factor, hormonal and metabolic regulation to yield longer GAG chains with altered structure and function. The mechanism by which the CS/DS GAG chains are polymerized is unknown. Recent work has identified several monosaccharide transferases which when co-expressed yield GAG polymers and the length of the polymers depends upon the pair of enzymes coexpressed. The further extension of these chains is regulated by signaling pathways. Inhibition of these latter pathways may be a therapeutic target to prevent the elongation which is associated with increased binding of atherogenic lipids and the disease process of atherosclerosis

Pathologic Features of the Intervertebral Disc in Young Nova Scotia Duck Tolling Retrievers Confirms Chondrodystrophy Degenerative Phenotype Associated With Genotype.

Chondrodystrophy results in predictable and progressive biochemical and structural changes to the intervertebral disc, resulting in early onset degeneration and dystrophic mineralization of the disc. Accelerated degeneration and mineralization of the intervertebral disc are common in multiple dog breeds and can result in compromised function, herniation, pain, and a variety of neurological sequelae. A mutation responsible for chondrodystrophy in dogs has been identified as an aberrant fibroblast growth factor 4 (FGF4) retrogene insertion on chromosome 12 (CFA12) and is associated with short stature of the Nova Scotia Duck Tolling Retriever. Segregation of the CFA12 FGF4 retrogene in this dog breed provides an opportunity to examine the effect of retrogene presence on radiographic and histologic appearance of chondrodystrophic disc degeneration within a single breed. Here we found that in the intervertebral discs isolated from 2 dogs with the CFA12 FGF4 genotype, the nucleus pulposus was largely replaced by cartilaginous tissue, and physaliferous notochordal cells were rarely if ever identified. These findings are in contrast to the normal histologic findings in 2 breed-matched dogs lacking the mutation. The findings are consistent with premature chondroid degeneration of the intervertebral disc and suggest that the presence of the CFA12 FGF4 retrogene is sufficient to cause the chondrodystrophic phenotype

Dependence of Na+/H+ antiport activation in cultured rat aortic smooth muscle on calmodulin, calcium, and ATP: evidence for the involvement of calmodulin-dependent kinases

The role of Ca2+/calmodulin-dependent processes in the activation of the Na+/H+ antiport of primary cultures of rat aortic smooth muscle was studied using 22Na+ uptake and measurement of intracellular pH (pHi) with the fluorescent pH dye 2',7'-bis-(2-carboxyethyl)-5(and 6)-carboxyfluorescein. Antiport activation following exposure to serum and by the induction of an intracellular acidosis could be markedly attenuated by calmodulin antagonists. Ionomycin also transiently elevated pHi and 5-(N-ethyl-N-isopropyl) amiloride-sensitive 22Na+ influx, effects consistent with activation of the antiport; these effects were abolished in cells exposed to calmodulin antagonists or [ethylenebis(oxyethylenenitrilo)]tetraacetic acid. Activation of the antiport following intracellular acidosis was markedly affected by cellular ATP depletion. A comparison of the abilities of control and 2-deoxy-D-glucose-treated cells to increase 5-(N-ethyl-N-isopropyl)amiloride-sensitive 22Na+ influx in response to graded acidifications indicated that attenuation of Na+/H+ antiport activity was due to both a shift of its pHi dependence and to a reduction in maximal activity. The results suggest that the Na+/H+ antiport of rat aortic smooth muscle is dependent on Ca2+/calmodulin-dependent processes, presumably phosphorylation, which influences its activity by modulating (i) an intracellular proton dependent regulatory mechanism (allosteric site) and (ii) the maximum activity of the antiport

Investigating the missing data mechanism in quality of life outcomes: a comparison of approaches

Background: Missing data is classified as missing completely at random (MCAR), missing at random (MAR) or missing not at random (MNAR). Knowing the mechanism is useful in identifying the most appropriate analysis. The first aim was to compare different methods for identifying this missing data mechanism to determine if they gave consistent conclusions. Secondly, to investigate whether the reminder-response data can be utilised to help identify the missing data mechanism. Methods: Five clinical trial datasets that employed a reminder system at follow-up were used. Some quality of life questionnaires were initially missing, but later recovered through reminders. Four methods of determining the missing data mechanism were applied. Two response data scenarios were considered. Firstly, immediate data only; secondly, all observed responses (including reminder-response). Results: In three of five trials the hypothesis tests found evidence against the MCAR assumption. Logistic regression suggested MAR, but was able to use the reminder-collected data to highlight potential MNAR data in two trials. Conclusion: The four methods were consistent in determining the missingness mechanism. One hypothesis test was preferred as it is applicable with intermittent missingness. Some inconsistencies between the two data scenarios were found. Ignoring the reminder data could potentially give a distorted view of the missingness mechanism. Utilising reminder data allowed the possibility of MNAR to be considered.The Chief Scientist Office of the Scottish Government Health Directorate. Research Training Fellowship (CZF/1/31