Trust in the police and affective evaluation of police faces: a preliminary study.

Introduction: A study was conducted to investigate if an individual's trust in law enforcement affects their perception of the emotional facial expressions displayed by police officers. Methods: The study invited 77 participants to rate the valence of 360 face images. Images featured individuals without headgear (condition 1), or with a baseball cap (condition 2) or police hat (condition 3) digitally added to the original photograph. The images were balanced across sex, race/ethnicity (Asian, African American, Latine, and Caucasian), and facial expression (Happy, Neutral, and Angry). After rating the facial expressions, respondents completed a survey about their attitudes toward the police. Results: The results showed that, on average, valence ratings for "Angry" faces were similar across all experimental conditions. However, a closer examination revealed that faces with police hats were perceived as angrier compared to the control conditions (those with no hat and those with a baseball cap) by individuals who held negative views of the police. Conversely, participants with positive attitudes toward the police perceived faces with police hats as less angry compared to the control condition. This correlation was highly significant for angry faces (p < 0.01), and stronger in response to male faces compared to female faces but was not significant for neutral or happy faces. Discussion: The study emphasizes the substantial role of attitudes in shaping social perception, particularly within the context of law enforcement.

Face processing and early event-related potentials: replications and novel findings.

This research explores early Event-Related Potentials (ERPs) sensitivity to facial stimuli, investigating various facial features aimed to unveil underlying neural mechanisms. Two experiments, each involving 15 undergraduate students, utilized a multidimensional stimulus set incorporating race, gender, age, emotional expression, face masks, and stimulus orientation. Findings highlight significant modulations in N170 and P200 amplitudes and latencies for specific attributes, replicating prior research and revealing novel insights. Notably, age-related facial feature variations, facial inversion, and the presence of face masks significantly impact neural responses. Several speculative explanations are proposed to elucidate these results: First, the findings lend support to the idea that the increased N170 amplitude observed with facial inversion is closely tied to the activation of object-sensitive neurons. This is further bolstered by a similar amplitude increase noted when masks (effective objects) are added to faces. Second, the absence of an additional amplitude increase, when inverting face images with face masks suggests that neural populations may have reached a saturation point, limiting further enhancement. Third, the study reveals that the latency deficit in N170 induced by facial inversion is even more pronounced in the subsequent ERP component, the P200, indicating that face inversion may impact multiple stages of face processing. Lastly, the significant increase in P200 amplitude, typically associated with face typicality, for masked faces in this study aligns with previous research that demonstrated elevated P200 amplitudes for scrambled faces. This suggests that obscured faces may be processed as typical, potentially representing a default state in face processing.

Affective evaluation of consciously perceived emotional faces reveals a "correct attribution effect".

The strength of the affective priming effect is influenced by various factors, including the duration of the prime. Surprisingly, short-duration primes that are around the threshold for conscious awareness typically result in stronger effects compared to long-duration primes. The misattribution effect theory suggest that subliminal primes do not provide sufficient cognitive processing time for the affective feeling to be attributed to the prime. Instead, the neutral target being evaluated is credited for the affective experience. In everyday social interactions, we shift our gaze from one face to another, typically contemplating each face for only a few seconds. It is reasonable to assume that no affective priming takes place during such interactions. To investigate whether this is indeed the case, participants were asked to rate the valence of faces displayed one by one. Each face image simultaneously served as both a target (primed by the previous trial) and a prime (for the next trial). Depending on the participant's response time, images were typically displayed for about 1-2 s. As predicted by the misattribution effect theory, neutral targets were not affected by positive affective priming. However, non-neutral targets showed a robust priming effect, with emotional faces being perceived as even more negative or positive when the previously seen face was emotionally congruent. These results suggest that a "correct attribution effect" modulates how we perceive faces, continuously impacting our social interactions. Given the importance of faces in social communication, these findings have wide-ranging implications.

Having Difficulties Reading the Facial Expression of Older Individuals? Blame It on the Facial Muscles, Not the Wrinkles.

Previous studies have found it is more difficult identifying an emotional expression displayed by an older than a younger face. It is unknown whether this is caused by age-related changes such as wrinkles and folds interfering with perception, or by the aging of facial muscles, potentially reducing the ability of older individuals to display an interpretable expression. To discriminate between these two possibilities, participants attempted to identify facial expressions under different conditions. To control for the variables (wrinkles/folds vs facial muscles), we used Generative Adversarial Networks to make faces look older or younger. Based upon behavior data collected from 28 individuals, our model predicts that the odds of correctly identifying the expressed emotion of a face reduced 16.2% when younger faces (condition 1) are artificially aged (condition 3). Replacing the younger faces with natural old-looking faces (Condition 2), however, results in an even stronger effect (odds of correct identification decreased by 50.9%). Counterintuitively, making old faces (Condition 2) look young (Condition 4) results in the largest negative effect (odds of correct identification decreased by 74.8% compared with natural young faces). Taken together, these results suggest that both age-related decline in the facial muscles' ability to express facial emotions and age-related physical changes in the face, explain why it is difficult to recognize facial expressions from older faces; the effect of the former, however, is much stronger than that of the latter. Facial muscle exercises, therefore, might improve the capacity to convey facial emotional expressions in the elderly.

Do Glasses Modulate Age Perception?

No formal studies have reported how glasses influence age perception, except for a London Vision Clinic survey that found that people over 45 look 5 or more years older when wearing eyeglasses. To investigate the effect of eyeglasses and sunglasses on age perception while controlling for age and interpersonal differences, we digitally manipulated the photographs of faces of 50 young adults, to create two age conditions (young and old) and three eyewear conditions (no glasses, eyeglasses, and sunglasses). Participants then estimated the age of the faces, displayed in random order. Contrary to the generally accepted beliefs that wearing eyeglasses makes you look older and wearing sunglasses make you look younger, our results suggest that the effect of glasses on age perception is rather small.

Human visual cortical gamma reflects natural image structure.

Many studies have reported visual cortical gamma-band activity related to stimulus processing and cognition. Most respective studies used artificial stimuli, and the few studies that used natural stimuli disagree. Electrocorticographic (ECoG) recordings from awake macaque areas V1 and V4 found gamma to be abundant during free viewing of natural images. In contrast, a study using ECoG recordings from V1 of human patients reported that many natural images induce no gamma and concluded that it is not necessary for seeing. To reconcile these apparently disparate findings, we reanalyzed those same human ECoG data recorded during presentation of natural images. We find that the strength of gamma is positively correlated with different image-computable metrics of image structure. This holds independently of the precise metric used to quantify gamma. In fact, an average of previously used gamma metrics reflects image structure most robustly. Gamma was sufficiently diagnostic of image structure to differentiate between any possible pair of images with >70% accuracy. Thus, while gamma might be weak for some natural images, the graded strength of gamma reflects the graded degree of image structure, and thereby conveys functionally relevant stimulus properties.

Dynamic encoding of face information in the human fusiform gyrus.

Humans' ability to rapidly and accurately detect, identify and classify faces under variable conditions derives from a network of brain regions highly tuned to face information. The fusiform face area (FFA) is thought to be a computational hub for face processing; however, temporal dynamics of face information processing in FFA remains unclear. Here we use multivariate pattern classification to decode the temporal dynamics of expression-invariant face information processing using electrodes placed directly on FFA in humans. Early FFA activity (50-75 ms) contained information regarding whether participants were viewing a face. Activity between 200 and 500 ms contained expression-invariant information about which of 70 faces participants were viewing along with the individual differences in facial features and their configurations. Long-lasting (500+ms) broadband gamma frequency activity predicted task performance. These results elucidate the dynamic computational role FFA plays in multiple face processing stages and indicate what information is used in performing these visual analyses.

Stimulus repetition modulates gamma-band synchronization in primate visual cortex.

When a sensory stimulus repeats, neuronal firing rate and functional MRI blood oxygen level-dependent responses typically decline, yet perception and behavioral performance either stay constant or improve. An additional aspect of neuronal activity is neuronal synchronization, which can enhance the impact of neurons onto their postsynaptic targets independent of neuronal firing rates. We show that stimulus repetition leads to profound changes of neuronal gamma-band (∼40-90 Hz) synchronization. Electrocorticographic recordings in two awake macaque monkeys demonstrated that repeated presentations of a visual grating stimulus resulted in a steady increase of visually induced gamma-band activity in area V1, gamma-band synchronization between areas V1 and V4, and gamma-band activity in area V4. Microelectrode recordings in area V4 of two additional monkeys under the same stimulation conditions allowed a direct comparison of firing rates and gamma-band synchronization strengths for multiunit activity (MUA), as well as for isolated single units, sorted into putative pyramidal cells and putative interneurons. MUA and putative interneurons showed repetition-related decreases in firing rate, yet increases in gamma-band synchronization. Putative pyramidal cells showed no repetition-related firing rate change, but a decrease in gamma-band synchronization for weakly stimulus-driven units and constant gamma-band synchronization for strongly driven units. We propose that the repetition-related changes in gamma-band synchronization maintain the interareal stimulus signaling and sharpen the stimulus representation by gamma-synchronized pyramidal cell spikes.

Ca(2+)-regulatory function of the inhibitory peptide region of cardiac troponin I is aided by the C-terminus of cardiac troponin T: Effects of familial hypertrophic cardiomyopathy mutations cTnI R145G and cTnT R278C, alone and in combination, on filament sliding.

Investigations of cardiomyopathy mutations in Ca(2+) regulatory proteins troponin and tropomyosin provide crucial information about cardiac disease mechanisms, and also provide insights into functional domains in the affected polypeptides. Hypertrophic cardiomyopathy-associated mutations TnI R145G, located within the inhibitory peptide (Ip) of human cardiac troponin I (hcTnI), and TnT R278C, located immediately C-terminal to the IT arm in human cardiac troponin T (hcTnT), share some remarkable features: structurally, biochemically, and pathologically. Using bioinformatics, we find compelling evidence that TnI and TnT, and more specifically the affected regions of hcTnI and hcTnT, may be related not just structurally but also evolutionarily. To test for functional interactions of these mutations on Ca(2+)-regulation, we generated and characterized Tn complexes containing either mutation alone, or both mutations simultaneously. The most important results from in vitro motility assays (varying [Ca(2+)], temperature or HMM density) show that the TnT mutant "rescued" some deleterious effects of the TnI mutant at high Ca(2+), but exacerbated the loss of function, i.e., switching off the actomyosin interaction, at low Ca(2+). Taken together, our experimental results suggest that the C-terminus of cTnT aids Ca(2+)-regulatory function of cTnI Ip within the troponin complex.

Robust gamma coherence between macaque V1 and V2 by dynamic frequency matching.

Current theories propose that coherence of oscillatory brain activity in the gamma band (30-80 Hz) constitutes an avenue for communication among remote neural populations. However, reports documenting stimulus dependency and time variability of gamma frequency suggest that distant neuronal populations may, at any one time, operate at different frequencies precluding synchronization. To test this idea, we recorded from macaque V1 and V2 simultaneously while presenting gratings of varying contrast. Although gamma frequency increased with stimulus contrast in V1 and V2 (by ∼25 Hz), V1-V2 gamma coherence was maintained for all contrasts. Moreover, while gamma frequency fluctuated by ∼15 Hz during constant contrast stimulation, this fluctuation was highly correlated between V1 and V2. The strongest coherence connections showed a layer-specific pattern, matching feedforward anatomical connectivity. Hence, gamma coherence among remote populations can occur despite large stimulus-induced and time-dependent changes in gamma frequency, allowing communication through coherence to operate without a stimulus independent, fixed-frequency gamma channel.

Micromechanical thermal assays of Ca2+-regulated thin-filament function and modulation by hypertrophic cardiomyopathy mutants of human cardiac troponin.

Microfabricated thermoelectric controllers can be employed to investigate mechanisms underlying myosin-driven sliding of Ca(2+)-regulated actin and disease-associated mutations in myofilament proteins. Specifically, we examined actin filament sliding-with or without human cardiac troponin (Tn) and α-tropomyosin (Tm)-propelled by rabbit skeletal heavy meromyosin, when temperature was varied continuously over a wide range (~20-63°C). At the upper end of this temperature range, reversible dysregulation of thin filaments occurred at pCa 9 and 5; actomyosin function was unaffected. Tn-Tm enhanced sliding speed at pCa 5 and increased a transition temperature (T(t)) between a high activation energy (E(a)) but low temperature regime and a low E(a) but high temperature regime. This was modulated by factors that alter cross-bridge number and kinetics. Three familial hypertrophic cardiomyopathy (FHC) mutations, cTnI R145G, cTnI K206Q, and cTnT R278C, cause dysregulation at temperatures ~5-8°C lower; the latter two increased speed at pCa 5 at all temperatures.

Facilitated cross-bridge interactions with thin filaments by familial hypertrophic cardiomyopathy mutations in α-tropomyosin.

Familial hypertrophic cardiomyopathy (FHC) is a disease of cardiac sarcomeres. To identify molecular mechanisms underlying FHC pathology, functional and structural differences in three FHC-related mutations in recombinant α-Tm (V95A, D175N, and E180G) were characterized using both conventional and modified in vitro motility assays and circular dichroism spectroscopy. Mutant Tm's exhibited reduced α-helical structure and increased unordered structure. When thin filaments were fully occupied by regulatory proteins, little or no motion was detected at pCa 9, and maximum speed (pCa 5) was similar for all tropomyosins. Ca(2+)-responsiveness of filament sliding speed was increased either by increased pCa(50) (V95A), reduced cooperativity n (D175N), or both (E180G). When temperature was increased, thin filaments with E180G exhibited dysregulation at temperatures ~10°C lower, and much closer to body temperature, than WT. When HMM density was reduced, thin filaments with D175N required fewer motors to initiate sliding or achieve maximum sliding speed.

Interaction between troponin and myosin enhances contractile activity of myosin in cardiac muscle.

Ca(2+) signaling in striated muscle cells is critically dependent upon thin filament proteins tropomyosin (Tm) and troponin (Tn) to regulate mechanical output. Using in vitro measurements of contractility, we demonstrate that even in the absence of actin and Tm, human cardiac Tn (cTn) enhances heavy meromyosin MgATPase activity by up to 2.5-fold in solution. In addition, cTn without Tm significantly increases, or superactivates sliding speed of filamentous actin (F-actin) in skeletal motility assays by at least 12%, depending upon [cTn]. cTn alone enhances skeletal heavy meromyosin's MgATPase in a concentration-dependent manner and with sub-micromolar affinity. cTn-mediated increases in myosin ATPase may be the cause of superactivation of maximum Ca(2+)-activated regulated thin filament sliding speed in motility assays relative to unregulated skeletal F-actin. To specifically relate this classical superactivation to cardiac muscle, we demonstrate the same response using motility assays where only cardiac proteins were used, where regulated cardiac thin filament sliding speeds with cardiac myosin are >50% faster than unregulated cardiac F-actin. We additionally demonstrate that the COOH-terminal mobile domain of cTnI is not required for this interaction or functional enhancement of myosin activity. Our results provide strong evidence that the interaction between cTn and myosin is responsible for enhancement of cross-bridge kinetics when myosin binds in the vicinity of Tn on thin filaments. These data imply a novel and functionally significant molecular interaction that may provide new insights into Ca(2+) activation in cardiac muscle cells.

Ca2+ sensitivity of regulated cardiac thin filament sliding does not depend on myosin isoform.

Myosin heavy chain (MHC) isoforms in vertebrate striated muscles are distinguished functionally by differences in chemomechanical kinetics. These kinetic differences may influence the cross-bridge-dependent co-operativity of thin filament Ca(2+) activation. To determine whether Ca(2+) sensitivity of unloaded thin filament sliding depends upon MHC isoform kinetics, we performed in vitro motility assays with rabbit skeletal heavy meromyosin (rsHMM) or porcine cardiac myosin (pcMyosin). Regulated thin filaments were reconstituted with recombinant human cardiac troponin (rhcTn) and alpha-tropomyosin (rhcTm) expressed in Escherichia coli. All three subunits of rhcTn were coexpressed as a functional complex using a novel construct with a glutathione S-transferase (GST) affinity tag at the N-terminus of human cardiac troponin T (hcTnT) and an intervening tobacco etch virus (TEV) protease site that allows purification of rhcTn without denaturation, and removal of the GST tag without proteolysis of rhcTn subunits. Use of this highly purified rhcTn in our motility studies resulted in a clear definition of the regulated motility profile for both fast and slow MHC isoforms. Maximum sliding speed (pCa 5) of regulated thin filaments was roughly fivefold faster with rsHMM compared with pcMyosin, although speed was increased by 1.6- to 1.9-fold for regulated over unregulated actin with both MHC isoforms. The Ca(2+) sensitivity of regulated thin filament sliding speed was unaffected by MHC isoform. Our motility results suggest that the cellular changes in isoform expression that result in regulation of myosin kinetics can occur independently of changes that influence thin filament Ca(2+) sensitivity.