Facial expressions affect the memory of facial colors.

Facial color influences the perception of facial expressions, and emotional expressions bias how facial color is remembered. However, it remains unclear whether facial expressions affect daily facial color memory. The memory color effect demonstrates that knowledge about typical colors affects the perception of the actual color of given objects. To investigate the effect of facial color memory, we examined whether the memory color effect for faces varies depending on facial expression. We calculated the subjective achromatic point of the facial expression image stimulus and compared the degree to which it was shifted from the actual achromatic point between facial expression conditions. We hypothesized that if the memory of facial color is influenced by the facial expression color (e.g., anger is a warm color, fear is a cold color), then the subjective achromatic point would vary with facial expression. In Experiment 1, we recruited 13 participants who adjusted the color of facial expression stimuli (anger, neutral, and fear) and a banana stimulus to be achromatic. No significant differences in the subjective achromatic point between facial expressions were observed. Subsequently, we conducted Experiment 2 with 23 participants because Experiment 1 did not account for the sensitivity to color changes on the face; humans perceive greater color differences in faces than in non-faces. Participants selected which facial color they believed the expression stimulus appeared to be, choosing one of two options provided to them. The results indicated that the subjective achromatic points of anger and fear faces significantly shifted toward the opposite color direction compared with neutral faces in the brief presentation condition. This research suggests that the memory color of faces differs depending on facial expressions and supports the idea that the perception of emotional expressions can bias facial color memory.

The effect of facial colour on implicit facial expressions.

Humans recognise reddish-coloured faces as angry. However, does facial colour also affect "implicit" facial expression perception of which humans are not explicitly aware? In this study, we investigated the effects of facial colour on implicit facial expression perception. The experimental stimuli were "hybrid faces", in which the low-frequency component of the neutral facial expression image was replaced with the low-frequency component of the facial expression image of happiness or anger. In Experiment 1, we confirmed that the hybrid face stimuli were perceived as neutral and, therefore, supported implicit facial expression perception. In Experiment 2, the hybrid face stimuli were adjusted to natural and reddish facial colours, and their friendliness ratings were compared. The results showed that the expression of happiness was rated as more friendly than the expression of anger. In addition, the expression of happiness was rated as friendlier when the low-frequency happy component was red, but the friendliness rating of the expression of anger did not change when it was presented in red. In Experiment 3, we affirmed the implicit facial expression perception even in reddish colours. These results suggest that facial colour modulates the perception of implicit facial expressions in hybrid facial stimuli.

Distinguishing mirror from glass: A "big data" approach to material perception.

Distinguishing mirror from glass is a challenging visual inference, because both materials derive their appearance from their surroundings, yet we rarely experience difficulties in telling them apart. Very few studies have investigated how the visual system distinguishes reflections from refractions and to date, there is no image-computable model that emulates human judgments. Here we sought to develop a deep neural network that reproduces the patterns of visual judgments human observers make. To do this, we trained thousands of convolutional neural networks on more than 750,000 simulated mirror and glass objects, and compared their performance with human judgments, as well as alternative classifiers based on "hand-engineered" image features. For randomly chosen images, all classifiers and humans performed with high accuracy, and therefore correlated highly with one another. However, to assess how similar models are to humans, it is not sufficient to compare accuracy or correlation on random images. A good model should also predict the characteristic errors that humans make. We, therefore, painstakingly assembled a diagnostic image set for which humans make systematic errors, allowing us to isolate signatures of human-like performance. A large-scale, systematic search through feedforward neural architectures revealed that relatively shallow (three-layer) networks predicted human judgments better than any other models we tested. This is the first image-computable model that emulates human errors and succeeds in distinguishing mirror from glass, and hints that mid-level visual processing might be particularly important for the task.

Gloss perception: Searching for a deep neural network that behaves like humans.

The visual computations underlying human gloss perception remain poorly understood, and to date there is no image-computable model that reproduces human gloss judgments independent of shape and viewing conditions. Such a model could provide a powerful platform for testing hypotheses about the detailed workings of surface perception. Here, we made use of recent developments in artificial neural networks to test how well we could recreate human responses in a high-gloss versus low-gloss discrimination task. We rendered >70,000 scenes depicting familiar objects made of either mirror-like or near-matte textured materials. We trained numerous classifiers to distinguish the two materials in our images-ranging from linear classifiers using simple pixel statistics to convolutional neural networks (CNNs) with up to 12 layers-and compared their classifications with human judgments. To determine which classifiers made the same kinds of errors as humans, we painstakingly identified a set of 60 images in which human judgments are consistently decoupled from ground truth. We then conducted a Bayesian hyperparameter search to identify which out of several thousand CNNs most resembled humans. We found that, although architecture has only a relatively weak effect, high correlations with humans are somewhat more typical in networks of shallower to intermediate depths (three to five layers). We also trained deep convolutional generative adversarial networks (DCGANs) of different depths to recreate images based on our high- and low-gloss database. Responses from human observers show that two layers in a DCGAN can recreate gloss recognizably for human observers. Together, our results indicate that human gloss classification can best be explained by computations resembling early to mid-level vision.

Cell-specific overexpression of COMT in dopaminergic neurons of Parkinson's disease.

The mechanism by which dopaminergic neurons are selectively affected in Parkinson's disease is not fully understood. In this study, we found a dramatic increase in the expression of catechol-O-methyltransferase (COMT), along with a lower level of DNA methylation, in induced pluripotent stem cell-derived dopaminergic neurons from patients with parkin (PARK2) gene mutations compared to those from healthy controls. In addition, a significant increase in the expression of COMT was found in dopaminergic neurons of isogenic PARK2 induced pluripotent stem cell lines that mimicked loss of function of PARK2 by CRISPR Cas9 technology. In dopamine transporter (DAT)-Cre mice, overexpression of COMT, specifically in dopaminergic neurons of the substantia nigra, produced cataleptic behaviours associated with impaired motor coordination. These findings suggest that upregulation of COMT, likely resulting from DNA hypomethylation, in dopaminergic neurons may contribute to the initial stage of neuronal dysfunction in Parkinson's disease.

Activation of ventral tegmental area dopaminergic neurons reverses pathological allodynia resulting from nerve injury or bone cancer.

Chronic pain induced by nerve damage due to trauma or invasion of cancer to the bone elicits severe ongoing pain as well as hyperalgesia and allodynia likely reflecting adaptive changes within central circuits that amplify nociceptive signals. The present study explored the possible contribution of the mesolimbic dopaminergic circuit in promoting allodynia related to neuropathic and cancer pain. Mice with ligation of the sciatic nerve or treated with intrafemoral osteosarcoma cells showed allodynia to a thermal stimulus applied to the paw on the injured side. Patch clamp electrophysiology revealed that the intrinsic neuronal excitability of ventral tegmental area (VTA) dopamine neurons projecting to the nucleus accumbens (N.Acc.) was significantly reduced in those mice. We used tyrosine hydroxylase (TH)-cre mice that were microinjected with adeno-associated virus (AAV) to express channelrhodopsin-2 (ChR2) to allow optogenetic stimulation of VTA dopaminergic neurons in the VTA or in their N.Acc. terminals. Optogenetic activation of these cells produced a significant but transient anti-allodynic effect in nerve injured or tumor-bearing mice without increasing response thresholds to thermal stimulation in sham-operated animals. Suppressed activity of mesolimbic dopaminergic neurons is likely to contribute to decreased inhibition of N.Acc. output neurons and to neuropathic or cancer pain-induced allodynia suggesting strategies for modulation of pathological pain states.

Effect of ghrelin on the motor deficit caused by the ablation of nigrostriatal dopaminergic cells or the inhibition of striatal dopamine receptors.

Ghrelin plays roles in a wide range of central functions by activating the growth hormone secretagogue receptor (GHSR). This receptor has recently been found in the substantia nigra (SN) to control dopamine (DA)-related physiological functions. The dysregulation of DA neurons in the SN pars compacta (SNc) and the consequent depletion of striatal DA are known to underlie the motor deficits observed in Parkinson's disease (PD). In the present study, we further investigated the role of the SN-ghrelin system in motor function under the stereotaxic injection of AAV-CMV-FLEX-diphtheria toxin A (DTA) into the SN of dopamine transporter (DAT)-Cre (DATSN::DTA) mice to expunge DA neurons of the SNc. First, we confirmed the dominant expression of GHSR1a, which is a functional GHSR, in tyrosine hydroxylase (TH)-positive DA neurons in the SNc of control mice. In DATSN::DTA mice, we clearly observed motor dysfunction using several behavioral tests. An immunohistochemical study revealed a dramatic loss of TH-positive DA neurons in the SNc and DAT-labeled axon terminals in the striatum, and an absence of mRNAs for TH and DAT in the SN of DATSN::DTA mice. The mRNA level of GHSR1a was drastically decreased in the SN of these mice. In normal mice, we also found the mRNA expression of GHSR1a within GABAergic neurons in the SN pars reticulata (SNr). Under these conditions, a single injection of ghrelin into the SN failed to improve the motor deficits caused by ablation of the nigrostriatal DA network using DATSN::DTA mice, whereas intra-SN injection of ghrelin suppressed the motor dysfunction caused by the administration of haloperidol, which is associated with the transient inhibition of DA transmission. These findings suggest that phasic activation of the SNc-ghrelin system could improve the dysregulation of nigrostriatal DA transmission related to the initial stage of PD, but not the motor deficits under the depletion of nigrostriatal DA. Although GHSRs are found in non-DA cells of the SNr, GHSRs on DA neurons in the SNc may play a crucial role in motor function.

ACTH stimulation test and computed tomography are useful for differentiating the subtype of primary aldosteronism.

The diagnostic steps for primary aldosteronism (PA) include case screening tests, confirmatory tests, and localization. The aim of this study was to identify useful confirmatory tests and their cut-off values for differentiating the subtype of primary aldosteronism, especially in unilateral PA, such as aldosterone-producing adenoma, and bilateral PA, such as idiopathic hyperaldosteronism. Seventy-six patients who underwent all four confirmatory tests, the captopril-challenge test (CCT), furosemide upright test (FUT), saline infusion test (SIT), and ACTH stimulation test (AST), and who were confirmed to have an aldosterone excess by adrenal venous sampling (AVS) were recruited. Subjects were diagnosed as having unilateral aldosterone excess (n=17) or bilateral aldosterone excess (n=59) by AVS. The SIT-positive rate was significantly higher in the unilateral group (94.1%) than in the bilateral group (57.6%). Multivariable logistic regression analysis showed that tumor on computed tomography (CT) and plasma aldosterone concentration (PAC)max/cortisol on the AST were useful for differentiating the subtype of PA. Receiver operating characteristic (ROC) curve analysis for distinguishing the subtype of PA showed that a cut-off value of 18.3 PACmax/cortisol on the AST had a sensitivity of 83% and a specificity of 88%. The area under the ROC curve was 0.918 (95% confidence interval 0.7916-0.9708). These data suggest that abdominal CT and AST are useful for differentiating the subtype of PA and the indication for AVS.

Robust brightness enhancement across a luminance range of the glare illusion.

The glare illusion refers to brightness enhancement and the perception of a self-luminous appearance that occurs when a central region is surrounded by a luminance gradient. The center region appears to be a light source, with its light dispersing into the surrounding region. If the luminous edge is critical for generating the illusion, modulating the perceived luminance of the image, and switching its appearance from luminous to nonluminous, would have a strong impact on lightness and brightness estimation. Here, we quantified the illusion in two ways, by assessing brightness enhancement and examining whether the center region appeared luminous. Thus, we could determine whether the two effects occurred jointly or independently. We examined a wide luminance range of center regions, from 0 to 200% relative to background. Brightness enhancement in the illusion was observed for a wide range of luminances (20% to 200% relative to background), while a luminous-white appearance was observed when the center region luminance was 145% of the background. These results exclude the possibility that brightness enhancement occurs because the stimuli appear self-luminous. We suggest that restoring the original image intensity precedes the perceptual process of lightness estimation.

[Pain and emotional dysregulation: Cellular memory due to pain].

Genetic factors are involved in determinants for the risk of psychiatric disorders, and neurological and neurodegenerative diseases. Chronic pain stimuli and intense pain have effects at a cellular and/or gene expression level, and will eventually induce "cellular memory due to pain", which means that tissue damage, even if only transient, can elicit epigenetically abnormal transcription/translation and post-translational modification in related cells depending on the degree or kind of injury or associated conditions. Such cell memory/transformation due to pain can cause an abnormality in a fundamental intracellular response, such as a change in the three-dimensional structure of DNA, transcription, or translation. On the other hand, pain is a multidimensional experience with sensory-discriminative and motivational-affective components. Recent human brain imaging studies have examined differences in activity in the nucleus accumbens between controls and patients with chronic pain, and have revealed that the nucleus accumbens plays a role in predicting the value of a noxious stimulus and its offset, and in the consequent changes in the motivational state. In this review, we provide a very brief overview of a comprehensive understanding of chronic pain associated with emotional dysregulation due to transcriptional regulation, epigenetic modification and miRNA regulation.

Glossiness perception and its pupillary response.

Recent studies have revealed that pupillary response changes depend on perceptual factors such as subjective brightness caused by optical illusions and luminance. However, the manner in which the perceptual factor that is derived from the glossiness perception of object surfaces affects the pupillary response remains unclear. We investigated the relationship between the glossiness perception and pupillary response through a glossiness rating experiment that included recording the pupil diameter. We prepared general object images (original) and randomized images (shuffled) that comprised the same images with randomized small square regions as stimuli. The image features were controlled by matching the luminance histogram. The observers were asked to rate the perceived glossiness of the stimuli presented for 3,000 ms and the changes in their pupil diameters were recorded. Images with higher glossiness ratings constricted the pupil size more than those with lower glossiness ratings at the peak constriction of the pupillary responses during the stimulus duration. The linear mixed-effects model demonstrated that the glossiness rating, image category (original/shuffled), variance of the luminance histogram, and stimulus area were most effective in predicting the pupillary responses. These results suggest that the illusory brightness obtained by the image regions of high-glossiness objects, such as specular highlights, induce pupil constriction.

Chronic ingestion of soy peptide supplementation reduces aggressive behavior and abnormal fear memory caused by juvenile social isolation.

Juvenile loneliness is a risk factor for psychopathology in later life. Deprivation of early social experience due to peer rejection has a detrimental impact on emotional and cognitive brain function in adulthood. Accumulating evidence indicates that soy peptides have many positive effects on higher brain function in rodents and humans. However, the effects of soy peptide use on juvenile social isolation are unknown. Here, we demonstrated that soy peptides reduced the deterioration of behavioral and cellular functions resulting from juvenile socially-isolated rearing. We found that prolonged social isolation post-weaning in male C57BL/6J mice resulted in higher aggression and impulsivity and fear memory deficits at 7 weeks of age, and that these behavioral abnormalities, except impulsivity, were mitigated by ingestion of soy peptides. Furthermore, we found that daily intake of soy peptides caused upregulation of postsynaptic density 95 in the medial prefrontal cortex and phosphorylation of the cyclic adenosine monophosphate response element binding protein in the hippocampus of socially isolated mice, increased phosphorylation of the adenosine monophosphate-activated protein kinase in the hippocampus, and altered the microbiota composition. These results suggest that soy peptides have protective effects against juvenile social isolation-induced behavioral deficits via synaptic maturation and cellular functionalization.

Processing of neuregulin-1 by neuropsin regulates GABAergic neuron to control neural plasticity of the mouse hippocampus.

Protease-mediated signaling is an important modulator of the nervous system. However, identifying the specific signaling substrates of such proteases is limited by the rapidity with which intermediate substrate forms are cleaved and released. Here, a screening method to detect noncleaved enzyme-bound forms was developed and used to identify a novel neuropsin/neuregulin-1 (NRG-1) proteolytic signaling system, which is specifically localized in the microdomain of synaptic cleft, in the mouse hippocampus. The extracellular protease, neuropsin, cleaved mature NRG-1 (comprising the extracellular domain of the NRG-1) at three newly identified sites to remove the heparin-binding domain of NRG-1. This released the ligand moiety from the matrix-glycosaminoglycan pool and enabled it to trigger the phosphorylation of NRG-1 receptor, p185 (ErbB4). Proteolysis of mature NRG-1 by neuropsin led to colocalization of the processed NRG-1 with ErbB4 in parvalbumin-positive hippocampal interneurons and consequent phosphorylation of tyrosine residues of proteins in the cells. Moreover, neuropsin knock-out mice exhibited impairments in Schaffer collateral early phase long-term potentiation, and application of the recombinant NRG-1 lacking heparin-binding activity reversed the effects through the activation of ErbB4 and GABA(A) receptors. Thus, ErbB4 signaling induced by neuropsin-dependent processing of NRG-1 contributes to the modulation of synaptic plasticity via regulation of GABAergic transmission. This signaling system may be involved in human cognition and mental disorders, such as schizophrenia and bipolar disorder, by its dysfunction.

Does extracellular proteolysis control mammalian cognition?

Recent advances in neuroscience techniques for analyzing synaptic functions, have revealed that even in a fully developed nervous system, dynamic structural changes in synapses can modify a variety of interactions between the presynaptic and postsynaptic neuron. Accumulating evidence suggests that extracellular proteases are involved in the structural modification of synapses through various pathways, including proteolytic cleavage at specific amino acid residues of the extracellular matrix proteins, cell adhesion molecules, and neurotrophic factors. Limited proteolysis induces changes in the properties of substrate proteins or releases functional domains (such as ligands) of the substrate proteins, which activate a signal transduction cascade, and hence could serve to initiate a variety of physiological functions. Such morphological and functional synaptic plasticity might underlie cognitive processes, including learning and memory in animals and humans. Here, we review potential molecular mechanisms of cognition-related focal proteolysis in the hippocampus. In addition, we developed a novel screening method to identify the physiological substrate for proteases.

Hollow cylindrical linear stator vibrator using a traveling wave of longitudinal axisymmetric vibration mode.

Ultrasonic motors (USMs) are expected to be used in special environments: high magnetic field environments and space environments, which require lightweight and multiple degrees of freedom. However, when used as linear ultrasonic motors (LUSMs), a linear guide and a preload mechanism are required, complicating the structure. In the present paper, a hollow cylindrical linear stator without an extra linear guide has been considered. The stator consists of a metal pipe and two piezoelectric (PZT) tubes installed at both ends of the metal pipe. Their connected parts are tapered for the first longitudinal axisymmetric vibration mode of the cylinder, namely L(0,1) mode excitation, and the metal pipe is subjected to radial strain. The vibration of the stator is assumed to be one-dimensional and is modeled by an electromechanical equivalent circuit. The principle that the traveling wave is formed on the metal pipe by dual-PZT-tube phase difference excitation was clarified. Finite element analysis and some measurements were conducted to confirm that the theory was consistent. The analyses and measurements were in good agreement. Therefore, the operating principle was confirmed. The results of the transport experiment showed that the average speed of the 8.5-g slider was 7.9 mm/s.

Elucidation of the mechanisms underlying tumor aggravation by the activation of stress-related neurons in the paraventricular nucleus of the hypothalamus.

A growing body of evidence suggests that excess stress could aggravate tumor progression. The paraventricular nucleus (PVN) of the hypothalamus plays an important role in the adaptation to stress because the hypothalamic-pituitary-adrenal (HPA) axis can be activated by inducing the release of corticotropin-releasing hormone (CRH) from the PVN. In this study, we used pharmacogenetic techniques to investigate whether concomitant activation of CRHPVN neurons could directly contribute to tumor progression. Tumor growth was significantly promoted by repeated activation of CRHPVN neurons, which was followed by an increase in the plasma levels of corticosterone. Consistent with these results, chronic administration of glucocorticoids induced tumor progression. Under the concomitant activation of CRHPVN neurons, the number of cytotoxic CD8+ T cells in the tumor microenvironment was dramatically decreased, and the mRNA expression levels of hypoxia inducible factor 1 subunit α (HIF1α), glucocorticoid receptor (GR) and Tsc22d3 were upregulated in inhibitory lymphocytes, tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs). Furthermore, the mRNA levels of various kinds of driver molecules related to tumor progression and tumor metastasis were prominently elevated in cancer cells by concomitant activation of CRHPVN neurons. These findings suggest that repeated activation of the PVN-CRHergic system may aggravate tumor growth through a central-peripheral-associated tumor immune system.

Identical germline mutations in the TMEM127 gene in two unrelated Japanese patients with bilateral pheochromocytoma.

OBJECTIVE: Recently, TMEM127 was shown to be a new pheochromocytoma susceptibility gene; this is consistent with its function as a tumour suppressor gene (Journal of Clinical Endocrinology and Metabolism, 2009, 94, 2817). Most pheochromocytomas arise from the adrenal medulla, and in approximately half of the cases, the tumours are bilateral (Journal of Clinical Endocrinology and Metabolism, 2009, 94, 2817; Journal of the American Medical Association, 2004, 292, 943; Human Mutation, 2010, 31, 41; Science, 2009, 325, 1139). The aim of the present study was to determine whether TMEM127 mutations are involved in the pathogenesis of pheochromocytomas/paragangliomas in Japanese subjects. PATIENTS AND METHODS: For this study, 74 unrelated patients with pheochromocytoma/paraganglioma who tested negative for mutations and deletions in RET, VHL, SDHB and SDHD were recruited through a multi-institutional collaborative effort in Japan. The TMEM127 gene sequence was determined in their germline DNA, and tumour DNA was analysed for the loss of heterozygosity. In addition, their TMEM127 gene sequences were compared with sequences from 114 normal healthy, ethnically matched controls. RESULTS: Among the 74 eligible patients, two unrelated patients (2·7%) with bilateral adrenal pheochromocytoma were found to have an identical germline TMEM127 mutation (c.116_119delTGTC, p.Ile41ArgfsX39) associated with 2q deletion loss of heterozygosity, which was also previously described in a Brazilian case (Journal of the American Medical Association, 2004, 292, 943). We also determined that none of the 114 normal healthy controls had this deletion mutation. CONCLUSION: This is the first report showing that TMEM127 mutation plays a pathological role in pheochromocytoma in an Asian population. Although our surveillance is limited, the prevalence and the phenotype of this gene mutation appear to be similar to those reported in previous studies.

Regularity of colour statistics in explaining colour composition preferences in art paintings.

This study explores the role of colour statistics in painting preferences and tests the 'matching-to-nature' hypothesis which posits that the preference for the colour composition of paintings depends on the extent to which the paintings resemble the colour statistics of natural scenes. A preference judgement experiment was conducted with 31,353 participants using original and hue-rotated versions of 1,200 paintings. Multiple regression analyses were performed between the measured preferences and paintings' colour statistics to reveal which colour statistics explained the preference data and to what extent. The colour statistics of art paintings that explained the preference data were compared to the colour statistics of natural scenes. The results identified the colour statistics that significantly contributed to explaining painting preferences, and the distributions of the paintings' colour statistics systematically differed from those of natural scenes. These findings suggest that the human visual system encodes colour statistics to make aesthetic judgements based on the artistic merit of colour compositions, and not on their similarity to natural scenes.

Investigation on substrate specificity and catalytic activity of serine protease neuropsin.

Neuropsin is one of serine proteases mainly found at the hippocampus and the amygdala, where it contributes to the long-term potentiation and memory acquisition by rebuilding of synaptic connections. Despite of the importance of neuropsin, the substrate specificity and regulation mechanisms of neuropsin have been unclear. Thus, we investigated the substrate specificity and the catalytic activity of neuropsin by the protein-ligand docking and molecular dynamics (MD) simulations and succeeded to reproduce the trend of the experimental results. Our study revealed that the substrate specificity and the activity of neuropsin depended on multiple factors: the substrate charge, the substrate orientation, the hydrogen bond network within the catalytic triad and the substrate, and the formation of the oxyanion hole. The apo neuropsin was not reactive without proper alignment of catalytic triad. The substrate binding induced the reactive alignment of catalytic triad. Then the substrate-neuropsin interaction forms the oxyanion hole that stabilizes the transition state and reduces the free-energy barrier of the following scission reaction.

Universality and superiority in preference for chromatic composition of art paintings.

Color composition in paintings is a critical factor affecting observers' aesthetic judgments. We examined observers' preferences for the color composition of Japanese and Occidental paintings when their color gamut was rotated. In the experiment, observers were asked to select their preferred image from original and three hue-rotated images in a four-alternative forced choice paradigm. Despite observers' being unfamiliar with the presented artwork, the original paintings (0 degrees) were preferred more frequently than the hue-rotated ones. Furthermore, the original paintings' superiority was observed when the images were divided into small square pieces and their positions randomized (Scrambled condition), and when the images were composed of square pieces collected from different art paintings and composed as patchwork images (Patchwork condition). Therefore, the original paintings' superiority regarding preference was quite robust, and the specific objects in the paintings associated with a particular color played only a limited role. Rather, the original paintings' general trend in color statistics influenced hue-angle preference. Art paintings likely share common statistical regulations in color distributions, which may be the basis for the universality and superiority of the preference for original paintings.