Moving through silence in dance: A neural perspective.

The word "silence" typically refers to the auditory modality, signifying an absence of sound or noise, being quiet. One may then ask: could we attribute the notion of silence to the domain of dance, e.g., when a movement is absent and the dancer stops moving? Is it at all useful to think in terms of silence when referring to dance? In this chapter, my exploration of these questions is based on recent studies in brain research, which demonstrate the remarkable facility of specific regions in the human brain to perceive visually referred biological and, in particular, human motion, leading to prediction of future movements of the human body. I will argue that merely ceasing motion is an insufficient condition for creating a perception of silence in the mind of a spectator of dance. Rather, the experience of silence in dance is a special situation where the static position of the dancer does not imply motion, and is unlikely to evoke interpretation of the intentions or the emotional expression of the dancer. For this to happen, the position of the dancer, while being still, should be held effortlessly, aimlessly, and with a minimal expression of emotion and intention. Furthermore, I suggest that dynamics, repetitive movement (such as that of Sufi whirling dervishes), can also be perceived as silence in dance because of the high level of predictability and evenness of the movement. These moments of silence in dance, which are so rare in our daily lives, invite us to experience the human body from a new, "out of the box" perspective that is the essence of all the arts.

Dancers' Somatic of Musicality.

Dancers often perform while synchronizing their movements to music, as required by the choreographer. In this article, we introduce the concept of categorizing choreography (or segments of it), according to its relationship with either the rhythm or the melody of the accompanied music, or with both. We demonstrate this distinction through several examples for each category. In a pilot study, we composed choreographic sequences that were either melodic-based or rhythmic-based and taught them to professional dancers. The results showed that some dancers tend to synchronize their movements better to rhythm and others, to melody. We refer to this tendency as the "dancers' somatic of musicality." The findings highlight important differences in the somatic of musicality among dancers, requiring attention from both choreographs and dancers, since these differences have bearing on the way dancers learn, memorize, and perform.

Abstracting Dance: Detaching Ourselves from the Habitual Perception of the Moving Body.

This work explores to what extent the notion of abstraction in dance is valid and what it entails. Unlike abstraction in the fine arts that aims for a certain independence from representation of the external world through the use of non-figurative elements, dance is realized by a highly familiar object - the human body. In fact, we are all experts in recognizing the human body. For instance, we can mentally reconstruct its motion from minimal information (e.g., via a "dot display"), predict body trajectory during movement and identify emotional expressions of the body. Nonetheless, despite the presence of a human dancer on stage and our extreme familiarity with the human body, the process of abstraction is applicable also to dance. Abstract dance removes itself from familiar daily movements, violates the observer's predictions about future movements and detaches itself from narratives. In so doing, abstract dance exposes the observer to perceptions of unfamiliar situations, thus paving the way to new interpretations of human motion and hence to perceiving ourselves differently in both the physical and emotional domains.

Macrophages dictate the progression and manifestation of hypertensive heart disease.

BACKGROUND: Inflammation has been implicated in the initiation, progression and manifestation of hypertensive heart disease. We sought to determine the role of monocytes/macrophages in hypertension and pressure overload induced left ventricular (LV) remodeling. METHODS AND RESULTS: We used two models of LV hypertrophy (LVH). First, to induce hypertension and LVH, we fed Sabra salt-sensitive rats with a high-salt diet. The number of macrophages increased in the hypertensive hearts, peaking at 10 weeks after a high-salt diet. Surprisingly, macrophage depletion, by IV clodronate (CL) liposomes, inhibited the development of hypertension. Moreover, macrophage depletion reduced LVH by 17% (p<0.05), and reduced cardiac fibrosis by 75%, compared with controls (p=0.001). Second, to determine the role of macrophages in the development and progression of LVH, independent of high-salt diet, we depleted macrophages in mice subjected to transverse aortic constriction and pressure overload. Significantly, macrophage depletion, for 3 weeks, attenuated LVH: a 12% decrease in diastolic and 20% in systolic wall thickness (p<0.05), and a 13% in LV mass (p=0.04), compared with controls. Additionally, macrophage depletion reduced cardiac fibrosis by 80% (p=0.006). Finally, macrophage depletion down-regulated the expression of genes associated with cardiac remodeling and fibrosis: transforming growth factor beta-1 (by 80%) collagen type III alpha-1 (by 71%) and atrial natriuretic factor (by 86%). CONCLUSIONS: Macrophages mediate the development of hypertension, LVH, adverse cardiac remodeling, and fibrosis. Macrophages, therefore, should be considered as a therapeutic target to reduce the adverse consequences of hypertensive heart disease.

What does the brain tell us about abstract art?

In this essay I focus on the question of why we are attracted to abstract art (perhaps more accurately, non-representational or object-free art). After elaborating on the processing of visual art in general and abstract art in particular, I discuss recent data from neuroscience and behavioral studies related to abstract art. I conclude with several speculations concerning our apparent appeal to this particular type of art. In particular, I claim that abstract art frees our brain from the dominance of reality, enabling it to flow within its inner states, create new emotional and cognitive associations, and activate brain-states that are otherwise harder to access. This process is apparently rewarding as it enables the exploration of yet undiscovered inner territories of the viewer's brain.

Exendin-4 promotes liver cell proliferation and enhances the PDX-1-induced liver to pancreas transdifferentiation process.

Over the last few years, evidence has accumulated revealing the unexpected potential of committed mammalian cells to convert to a different phenotype via a process called transdifferentiation or adult cell reprogramming. These findings may have major practical implications because this process may facilitate the generation of functional autologous tissues that can be used for replacing malfunctioning organs. An instructive role for transcription factors in diverting the developmental fate of cells in adult tissues has been demonstrated when adult human liver cells were induced to transdifferentiate to the pancreatic endocrine lineage upon ectopic expression of the pancreatic master regulator PDX-1 (pancreatic and duodenal homeobox gene 1). Since organogenesis and lineage commitment are affected also by developmental signals generated in response to environmental triggers, we have now analyzed whether the hormone GLP-1 (glucogen-like peptide-1) documented to play a role in pancreatic beta cell differentiation, maturation, and survival, can also increase the efficiency of liver to pancreas transdifferentiation. We demonstrate that the GLP-1R agonist, exendin-4, significantly improves the efficiency of PDX-1-mediated transdifferentiation. Exendin-4 affects the transdifferentiation process at two distinct steps; it increases the proliferation of liver cells predisposed to transdifferentiated in response to PDX-1 and promotes the maturation of transdifferentiated cells along the pancreatic lineage. Liver cell reprogramming toward the pancreatic beta cell lineage has been suggested as a strategy for functional replacement of the ablated insulin-producing cells in diabetics. Understanding the cellular and molecular basis of the transdifferentiation process will allow us to increase the efficiency of the reprogramming process and optimize its therapeutic merit.

Pancreatic and duodenal homeobox gene 1 induces hepatic dedifferentiation by suppressing the expression of CCAAT/enhancer-binding protein beta.

UNLABELLED: It is believed that adult tissues in mammals lack the plasticity needed to assume new developmental fates because of the absence of efficient pathways of dedifferentiation. However, the well-documented ability of the transcription factor pancreatic and duodenal homeobox gene 1 (PDX-1) to activate pancreatic lineage development and insulin production following ectopic expression in liver suggests a surprising degree of residual plasticity in adult liver cells. This study seeks a mechanistic explanation for the capacity of PDX-1 to endow liver cells with pancreatic characteristics and function. We demonstrate that PDX-1, previously shown to play an essential role in normal pancreatic organogenesis and pancreatic beta-cell function and to possess the potential to activate multiple pancreatic markers in liver, can also direct hepatic dedifferentiation. PDX-1 represses the adult hepatic repertoire of gene expression and activates the expression of the immature hepatic marker alpha-fetoprotein. We present evidence indicating that PDX-1 triggers hepatic dedifferentiation by repressing the key hepatic transcription factor CCAAT/enhancer-binding protein beta. Hepatic dedifferentiation is necessary though not sufficient for the activation of the mature pancreatic repertoire in liver. CONCLUSION: Our study suggests a dual role for PDX-1 in liver: inducing hepatic dedifferentiation and activating the pancreatic lineage. The identification of dedifferentiation signals may promote the capacity to endow mature tissues in mammals with the plasticity needed for acquiring novel developmental fates and functions to be implemented in the field of regenerative medicine.