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This music score was submitted for Resonate 2024: An Open Access Call for Scores by the UCLA Music Library.

This music score was submitted for Resonate 2024: An Open Access Call for Scores by the UCLA Music Library with Bent Frequency and Jan Berry Baker.

This music score was submitted for Resonate 2024: An Open Access Call for Scores by the UCLA Music Library.

In many team-based activities, members search for information to gain situational awareness and thereby structure their own behavior. The extent to which members are coupled and in control of their surrounding environment can be accessed via the fluctuations of their searching behaviors. To facilitate prospective control, assistive technologies such as a head-up display (HUD) can alleviate the demands of search and facilitate team performance. This study investigated how three-person teams divided their labor and structured their search behavior when playing a multiplayer search-and-retrieval task where first-person visibility and access to a HUD were manipulated. Results showed that access to task relevant information facilitated performance and division of labor, and increased prospective control of searching behaviors, as indexed by detrended fluctuation analysis (DFA). Over multiple sessions, teams learned to use the HUD to structure their behavior to achieve the task goal. Results indicate the potential in using DFA for monitoring prospective control in team contexts.

This music score was submitted for the Kaleidoscope 2020 Call for Scores, an open access collaboration with the UCLA Music Library.

This music score was submitted for the Kaleidoscope 2020 Call for Scores, an open access collaboration with the UCLA Music Library.

This music score was submitted for the Kaleidoscope 2020 Call for Scores, an open access collaboration with the UCLA Music Library.

We investigate the joint moments of derivatives of characteristic polynomials over the unitary symplectic group S p (2 N) and the orthogonal ensembles S O (2 N) and O − (2 N) . We prove asymptotic formulae for the joint moments of the n 1th and n 2th derivatives of the characteristic polynomials for all three matrix ensembles. Our results give two explicit formulae for each of the leading order coefficients, one in terms of determinants of hypergeometric functions and the other as combinatorial sums over partitions. We use our results to put forward conjectures on the joint moments of derivatives of L -functions with symplectic and orthogonal symmetry. [ABSTRACT FROM AUTHOR]

In a series of 6 experiments, two hypotheses were tested: that nominal heading perception is determined by the relative motion of images of objects positioned at different depths (R. F. Wang & J. E. Cutting, 1999) and that static depth information contributes to this determination. By manipulating static depth information while holding retinal-image motion constant during simulated self-movement, the authors found that static depth information played a role in determining perceived heading. Some support was also found for the involvement of R. F. Wang and J. E. Cutting's (1999) categories of object-image relative motion in determining perceived heading. However, results suggested an unexpected functional dominance of information about heading relative to apparently near objects.

The classically recognized functions of the renin-angiotensin system are mediated by type 1 ([AT.sub.1]) angiotensin receptors. Whereas man possesses a single [AT.sub.1] receptor, there are two [AT.sub.1] receptor isoforms in rodents ([AT.sub.1A] and [AT.sub.1B]) that are products of separate genes (Agtr1a and Agtr1b). We have generated mice lacking [AT.sub.1B] (Agtr1b -/-) and both [AT.sub.1A] and [AT.sub.1B] receptors (Agtr1a -/-Agtr1b -/-). Agtr1b -/- mice are healthy, without an abnormal phenotype. In contrast, Agtr1a -/-Agtr1b -/- mice have diminished growth, vascular thickening within the kidney, and atrophy of the inner renal medulla. This phenotype is virtually identical to that seen in angiotensinogen-deficient (Agt-/-) and angiotensin-converting enzyme-deficient (Ace -/-) mice that are unable to synthesize angiotensin II. Agtr1a -/-Agtr1b -/- mice have no systemic pressor response to infusions of angiotensin II, but they respond normally to another vasoconstrictor, epinephrine. Blood pressure is reduced substantially in the Agtr1a -/- Agtr1b -/- mice and following administration of an angiotensin converting enzyme inhibitor, their blood pressure increases paradoxically. We suggest that this is a result of interruption of [AT.sub.2]-receptor signaling. In summary, our studies suggest that both A[T.sub.1] receptors promote somatic growth and maintenance of normal kidney structure. The absence of either of the [AT.sub.1] receptor isoforms alone can be compensated in varying degrees by the other isoform. These studies reaffirm and extend the importance of [AT.sub.1] receptors to mediate physiological functions of the renin-angiotensin system.

F2 progeny from a series of crosses between F1 mice that were heterozygous for a targeted disruption of the type 1A angiotensin (AT(sub 1A)) receptor gene were studied to investigate the function of the AT(sub 1A) receptor in renal growth and development. Findings indicated that the genetic absence of AT(sub 1A) receptors in mouse results in a slight but significant survival disadvantage. In surviving F2 Agtr1A-(-/-) mice, somatic and renal growth and development were normal, although some of the adult Agtr1A-(-/-) mice had slight mesangial expansion.

The role of angiotensin AT1A and AT1B receptors in the regulation of blood pressure in response to angiotensin (ANG) II were analyzed in AT1A receptor-deficient (Agtr1A -/-) mice. Analysis of the mechanisms of ANG II activity on vascular tone in AgtrA1 -/- mice indicated the role of the AgtrA1 receptor gene in regulating blood pressure. Furthermore, the AgrA1 receptor gene also mediated hemodynamic responses to exogenous ANG II.

Oliverio, Michael I., Marielle Delnomdedieu, Christopher F. Best, Ping Li, Mariana Morris, Michael F. Callahan, G. Allan Johnson, Oliver Smithies, and Thomas M. Coffman. Abnormal water metabolism in mice lacking the type 1A receptor for ANG II. Am. J. Physiol. Renal Physiol. 278: F75-F82, 2000.--Mice lacking [AT.sub.1A] receptors for ANG II have a defect in urinary concentration manifested by an inability to increase urinary osmolality to levels seen in controls after thirsting. This defect results in extreme serum hypertonicity during water deprivation. In the basal state, plasma vasopressin levels are similar in wild-type controls and Agtr1a -/- mice. Plasma vasopressin levels increase normally in the [AT.sub.1A] receptor-deficient mice after 24 h of water deprivation, suggesting that the defect in urine concentration is intrinsic to the kidney. Using magnetic resonance microscopy, we find that the absence of [AT.sub.1A] receptors is associated with a modest reduction in the distance from the kidney surface to the tip of the papilla. However, this structural abnormality seems to play little role in the urinary concentrating defect in Agtr1a -/- mice since the impairment is largely reproduced in wild-type mice by treatment with an [AT.sup.1]-receptor antagonist. These studies demonstrate a critical role for the [AT.sup.1A] receptor in maintaining inner medullary structures in the kidney and in regulating renal water excretion. gene targeting; urinary concentration; magnetic resonance microscopy; papilla; vasopressin