People underestimate the numerosity of collections in which a few dots are connected in pairs by task-irrelevant lines. Such configural processing suggests that visual numerosity depends on the perceived scene segments, rather than on the perceived total area occupied by a collection. However, a methodology that uses irrelevant line connections may also introduce unnecessary distraction and variety, or obscure the perception of task-relevant items, given the saliency of the lines. To avoid such potentially confounding variables, we conducted four experiments where the line-connected dots were replaced with collinear inducers of Kanizsa-type illusory contours. Our participants had to compare two simultaneously presented collections and choose the more numerous one. Displays comprised c-shaped inducers and disks (Experiment 1), c-shaped inducers only (Experiments 2 and 4), or closed inducers (Experiment 3). One display always showed a 12- (Experiments 1-3) or 48-item reference pattern (Experiment 4); the other was a test pattern with numerosity varying between 9 and 15 (Experiments 1-3) or 36-60 items (Experiment 4). By manipulating the number of illusory contours in the test patterns, the level of connectedness increased or decreased respectively. The fitted psychometric functions revealed an underestimation that increased with the number of illusory contours in Experiments 1 and 2, but was absent in Experiments 3 and 4, where illusory contours were more difficult to perceive or larger numerosities were used. Results corroborate claims that visual numerosity estimation depends on segmented inputs, but only within moderate numerical ranges.
Summary:The levels of protein kinase C-␥ (PKC-␥ ) and the calcium/calmodulin-dependent kinase II-␣ (CaMKII-␣ ) were measured in crude synaptosomal (P2), particulate (P3), and cytosolic (S3) fractions of the neocortex of rats exposed to 1-hour and 2-hour middle cerebral artery occlusion (MCAO) and 2-hour MCAO followed by 2-hour reperfusion. During MCAO, PKC levels increased in P2 and P3 in the most severe ischemic areas concomitantly with a decrease in S3. In the penumbra, PKC␥ decreased in S3 without any significant increases in P2 and P3. Total PKC-␥ also decreased in the penumbra but not in the ischemic core, suggesting that the protein is degraded by an energy-dependent mechanism, possibly by the 26S proteasome. The CaMKII-␣ levels increased in P2 but not P3 during ischemia and reperfusion in all ischemic regions, particularly in the ischemic core. Concomitantly, the levels in S3 decreased by 20% to 40% in the penumbra and by approximately 80% in the ischemic core. There were no changes in the total levels of CaMKII-␣ during MCAO. The authors conclude that during and after ischemia, PKC and CaMKII-␣ are translocated to the cell membranes, particularly synaptic membranes, where they may modulate cellular function, such as neurotransmission, and also affect cell survival. Drugs preventing PKC and/or CaMKII-␣ translocation may prove beneficial against ischemic cell death.
Sterol regulatory element-binding protein-1 (SREBP-1) plays a central role in transcriptional regulation of genes for hepatic lipid synthesis that utilizes diet-derived nutrients such as carbohydrates and amino acids, and expression of SREBP-1 exhibits daily rhythms with a peak in the nocturnal feeding period under standard housing conditions of mice. Here, we report that the Srebp-1 expression rhythm shows time cue-independent and Clock mutation-sensitive circadian nature, and is synchronized with varied photoperiods apparently through entrainment of locomotor activity and food intake. Fasting caused diminution of Srebp-1 expression, while diabetic db/db and ob/ob mice showed constantly high expression with loss of rhythmicity. Time-restricted feedings during mid-light and mid-dark periods exhibited differential effects, the latter causing more severe damping of the oscillation. Therefore, "when to eat in a day (the light/dark cycle)," rather than "whenever to eat in a day," is a critical determinant to shape the daily rhythm of Srebp-1 expression. We further found that a high-carbohydrate diet and a high-protein diet, as well as a high-fat diet, cause phase shifts of the oscillation peak into the light period, underlining the importance of "what to eat." Daily rhythms of SREBP-1 protein levels and Akt phosphorylation levels also exhibited nutrientresponsive changes. Taken together, these findings provide a model for mechanisms by which time of day and nutrients in feeding shape daily rhythms of the Srebp-1 expression and possibly a number of other physiological functions with interindividual and interdaily differences in human beings and wild animals subjected to day-by-day changes in dietary timing and nutrients.The circadian timekeeping system for physiology and behavior in mammals consists of a whole-body network of cell-intrinsic oscillators that rely on activation/repression-alternating feedback loops of clock gene expression (1, 2). Daily expression rhythms of clock genes as oscillation generators are synchronized (entrained) to the light/dark cycle in the central pacemaker localized to the suprachiasmatic nucleus (SCN) 3 of the hypothalamus, whereas they are predominantly entrained to the feeding/fasting cycle in other brain regions and peripheral organs (3-5). On the other hand, it is poorly understood how daily rhythms of a large number of physiological functions as oscillation outputs are shaped and coordinated with each other.As a typical example of daily rhythms of liver functions exhibiting a wide spectrum of variety, we (6, 7) previously studied regulatory mechanisms for daily expression rhythms of the gene encoding Spot14 (8, 9) a regulatory protein stimulating lipid biosynthesis that is one of the most closely feeding-related functions in the liver. Because the Spot14 promoter is under the control (10) of sterol regulatory element-binding protein (SREBP)-1c (11, 12) a pivotal transcriptional regulator of genes for triglyceride synthesis, we here focused on Srebp-1 expression rhythms in the mous...
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