Empathy, engagement, entrainment: the interaction dynamics of aesthetic experience

A recent version of the view that aesthetic experience is based in empathy as inner imitation explains aesthetic experience as the automatic simulation of actions, emotions, and bodily sensations depicted in an artwork by motor neurons in the brain. Criticizing the simulation theory for committing to an erroneous concept of empathy and failing to distinguish regular from aesthetic experiences of art, I advance an alternative, dynamic approach and claim that aesthetic experience is enacted and skillful, based in the recognition of others’ experiences as distinct from one’s own. In combining insights from mainly psychology, phenomenology, and cognitive science, the dynamic approach aims to explain the emergence of aesthetic experience in terms of the reciprocal interaction between viewer and artwork. I argue that aesthetic experience emerges by participatory sense-making and revolves around movement as a means for creating meaning. While entrainment merely plays a preparatory part in this, aesthetic engagement constitutes the phenomenological side of coupling to an artwork and provides the context for exploration, and eventually for moving, seeing, and feeling with art. I submit that aesthetic experience emerges from bodily and emotional engagement with works of art via the complementary processes of the perception–action and motion–emotion loops. The former involves the embodied visual exploration of an artwork in physical space, and progressively structures and organizes visual experience by way of perceptual feedback from body movements made in response to the artwork. The latter concerns the movement qualities and shapes of implicit and explicit bodily responses to an artwork that cue emotion and thereby modulate over-all affect and attitude. The two processes cause the viewer to bodily and emotionally move with and be moved by individual works of art, and consequently to recognize another psychological orientation than her own, which explains how art can cause feelings of insight or awe and disclose aspects of life that are unfamiliar or novel to the viewer

Impact of leg lengthening on viscoelastic properties of the deep fascia

<p>Abstract</p> <p>Background</p> <p>Despite the morphological alterations of the deep fascia subjected to leg lengthening have been investigated in cellular and extracellular aspects, the impact of leg lengthening on viscoelastic properties of the deep fascia remains largely unknown. This study aimed to address the changes of viscoelastic properties of the deep fascia during leg lengthening using uniaxial tensile test.</p> <p>Methods</p> <p>Animal model of leg lengthening was established in New Zealand white rabbits. Distraction was initiated at a rate of 1 mm/day and 2 mm/day in two steps, and preceded until increases of 10% and 20% in the initial length of tibia had been achieved. The deep fascia specimens of 30 mm × 10 mm were clamped with the Instron 1122 tensile tester at room temperature with a constant tensile rate of 5 mm/min. After 5 load-download tensile tests had been performed, the specimens were elongated until rupture. The load-displacement curves were automatically generated.</p> <p>Results</p> <p>The normal deep fascia showed typical viscoelastic rule of collagenous tissues. Each experimental group of the deep fascia after leg lengthening kept the properties. The curves of the deep fascia at a rate of 1 mm/day with 20% increase in tibia length were the closest to those of normal deep fascia. The ultimate tension strength and the strain at rupture on average of normal deep fascia were 2.69 N (8.97 mN/mm²) and 14.11%, respectively. The increases in ultimate tension strength and strain at rupture of the deep fascia after leg lengthening were statistically significant.</p> <p>Conclusion</p> <p>The deep fascia subjected to leg lengthening exhibits viscoelastic properties as collagenous tissues without lengthening other than increased strain and strength. Notwithstanding different lengthening schemes result in varied viscoelastic properties changes, the most comparable viscoelastic properties to be demonstrated are under the scheme of a distraction rate of 1 mm/day and 20% increase in tibia length.</p

Gipc3 mutations associated with audiogenic seizures and sensorineural hearing loss in mouse and human

Sensorineural hearing loss affects the quality of life and communication of millions of people, but the underlying molecular mechanisms remain elusive. Here, we identify mutations in Gipc3 underlying progressive sensorineural hearing loss (age-related hearing loss 5, ahl5) and audiogenic seizures (juvenile audiogenic monogenic seizure 1, jams1) in mice and autosomal recessive deafness DFNB15 and DFNB95 in humans. Gipc3 localizes to inner ear sensory hair cells and spiral ganglion. A missense mutation in the PDZ domain has an attenuating effect on mechanotransduction and the acquisition of mature inner hair cell potassium currents. Magnitude and temporal progression of wave I amplitude of afferent neurons correlate with susceptibility and resistance to audiogenic seizures. The Gipc3343A allele disrupts the structure of the stereocilia bundle and affects long-term function of auditory hair cells and spiral ganglion neurons. Our study suggests a pivotal role of Gipc3 in acoustic signal acquisition and propagation in cochlear hair cells

Expression of NF-κB p50 in Tumor Stroma Limits the Control of Tumors by Radiation Therapy

Radiation therapy aims to kill cancer cells with a minimum of normal tissue toxicity. Dying cancer cells have been proposed to be a source of tumor antigens and may release endogenous immune adjuvants into the tumor environment. For these reasons, radiation therapy may be an effective modality to initiate new anti-tumor adaptive immune responses that can target residual disease and distant metastases. However, tumors engender an environment dominated by M2 differentiated tumor macrophages that support tumor invasion, metastases and escape from immune control. In this study, we demonstrate that following radiation therapy of tumors in mice, there is an influx of tumor macrophages that ultimately polarize towards immune suppression. We demonstrate using in vitro models that this polarization is mediated by transcriptional regulation by NFκB p50, and that in mice lacking NFκB p50, radiation therapy is more effective. We propose that despite the opportunity for increased antigen-specific adaptive immune responses, the intrinsic processes of repair following radiation therapy may limit the ability to control residual disease

The Neuropeptide Allatostatin A Regulates Metabolism and Feeding Decisions in Drosophila

Coordinating metabolism and feeding is important to avoid obesity and metabolic diseases, yet the underlying mechanisms, balancing nutrient intake and metabolic expenditure, are poorly understood. Several mechanisms controlling these processes are conserved in Drosophila, where homeostasis and energy mobilization are regulated by the glucagon-related adipokinetic hormone (AKH) and the Drosophila insulin-like peptides (DILPs). Here, we provide evidence that the Drosophila neuropeptide Allatostatin A (AstA) regulates AKH and DILP signaling. The AstA receptor gene, Dar-2, is expressed in both the insulin and AKH producing cells. Silencing of Dar-2 in these cells results in changes in gene expression and physiology associated with reduced DILP and AKH signaling and animals lacking AstA accumulate high lipid levels. This suggests that AstA is regulating the balance between DILP and AKH, believed to be important for the maintenance of nutrient homeostasis in response to changing ratios of dietary sugar and protein. Furthermore, AstA and Dar-2 are regulated differentially by dietary carbohydrates and protein and AstA-neuronal activity modulates feeding choices between these types of nutrients. Our results suggest that AstA is involved in assigning value to these nutrients to coordinate metabolic and feeding decisions, responses that are important to balance food intake according to metabolic needs

Persistence in eye movement during visual search

As any cognitive task, visual search involves a number of underlying processes that cannot be directly observed and measured. In this way, the movement of the eyes certainly represents the most explicit and closest connection we can get to the inner mechanisms governing this cognitive activity. Here we show that the process of eye movement during visual search, consisting of sequences of fixations intercalated by saccades, exhibits distinctive persistent behaviors. Initially, by focusing on saccadic directions and intersaccadic angles, we disclose that the probability distributions of these measures show a clear preference of participants towards a reading-like mechanism (geometrical persistence), whose features and potential advantages for searching/foraging are discussed. We then perform a Multifractal Detrended Fluctuation Analysis (MF-DFA) over the time series of jump magnitudes in the eye trajectory and find that it exhibits a typical multifractal behavior arising from the sequential combination of saccades and fixations. By inspecting the time series composed of only fixational movements, our results reveal instead a monofractal behavior with a Hurst exponent [Image: see text], which indicates the presence of long-range power-law positive correlations (statistical persistence). We expect that our methodological approach can be adopted as a way to understand persistence and strategy-planning during visual search

C1 lateral mass screw-induced occipital neuralgia: a report of two cases

C1–2 polyaxial screw-rod fixation is a relatively new technique. While recognizing the potential for inadvertent vertebral artery injury, there have been few reports in the literature outlining all the possible complications. Aim of this study is to review all cases of C1 lateral mass screws insertion with emphasis on the evaluation of potential structures at risk during the procedure. We retrospectively reviewed all patients in our unit who had C1 lateral mass screw insertion over a 2-year period. The C1 lateral mass screw was inserted as part of an atlantoaxial stabilization or incorporated into a modular occiput/subaxial construct. Outcome measures included clinical and radiological parameters. Clinical indicators included age, gender, neurologic status, surgical indication and the number of levels stabilized. Intraoperative complications including blood loss, vertebral artery injury or dural tears were recorded. Postoperative pain distribution and neurological deficit were recorded. Radiological indicators included postoperative plain radiographs to assess sagittal alignment and to check for screw malposition or construct failure. A total of 18 lateral mass screws were implanted in 9 patients. There were three male and six female patients who had C1 lateral mass screw insertion in this unit. Two patients had atlantoaxial stabilization for C2 fracture. There were four patients with rheumatoid arthritis whose C1 lateral mass screws were inserted as part of an occipitocervical or subaxial cervical stabilization. There was no vertebral artery injury, no cerebrospinal fluid leak and minimal blood loss in all patients. Three patients developed postoperative occipital neuralgia. This neuralgia was transient, in one of the patients having settled at 6-week follow-up. In the other two patients the neuralgia was unresolved at time of latest follow-up but was adequately controlled with appropriate pain management. Postoperatively no patient had radiographic evidence of construct failure and all demonstrated excellent sagittal alignment. It has been reported that the absence of threads on the upper portion of the long shank screw may protect against neural irritation. However, insertion of the C1 lateral mass screw necessitates careful caudal retraction of the C2 dorsal root ganglion. The insertion point for the C1 lateral mass screw is at the junction of the C1 posterior arch and the midpoint of the posterior inferior part of the C1 lateral mass. Two patients in our series suffered occipital neuralgia post-insertion of C1 lateral mass screws. This highlights the potential for damage to the C2 nerve root during C1 lateral mass screw placement