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Saccades to single targets in peripheral vision are typically characterized by an undershoot bias. Putting this bias to a test, Kapoula [1] used a paradigm in which observers were presented with two different sets of target eccentricities that partially overlapped each other. Her data were suggestive of a saccadic range effect (SRE): There was a tendency for saccades to overshoot close targets and undershoot far targets in a block, suggesting that there was a response bias towards the center of eccentricities in a given block. Our Experiment 1 was a close replication of the original study by Kapoula [1]. In addition, we tested whether the SRE is sensitive to top-down requirements associated with the task, and we also varied the target presentation duration. In Experiments 1 and 2, we expected to replicate the SRE for a visual discrimination task. The simple visual saccade-targeting task in Experiment 3, entailing minimal top-down influence, was expected to elicit a weaker SRE. Voluntary saccades to remembered target locations in Experiment 3 were expected to elicit the strongest SRE. Contrary to these predictions, we did not observe a SRE in any of the tasks. Our findings complement the results reported by Gillen et al. [2] who failed to find the effect in a saccade-targeting task with a very brief target presentation. Together, these results suggest that unlike arm movements, saccadic eye movements are not biased towards making saccades of a constant, optimal amplitude for the task.
Since years, research on SnRK1, the major cellular energy sensor in plants, has tried to define its role in energy signalling. However, these attempts were notoriously hampered by the lethality of a complete knockout of SnRK1. Therefore, we generated an inducible amiRNA:: SnRK1 alpha 2 in a snrk1 alpha 1 knock out background (snrk1 alpha 1/alpha 2) to abolish SnRK1 activity to understand major systemic functions of SnRK1 signalling under energy deprivation triggered by extended night treatment. We analysed the in vivo phosphoproteome, proteome and metabolome and found that activation of SnRK1 is essential for repression of high energy demanding cell processes such as protein synthesis. The most abundant effect was the constitutively high phosphorylation of ribosomal protein S6 (RPS6) in the snrk1 alpha 1/alpha 2 mutant. RPS6 is a major target of TOR signalling and its phosphorylation correlates with translation. Further evidence for an antagonistic SnRK1 and TOR crosstalk comparable to the animal system was demonstrated by the in vivo interaction of SnRK1 alpha 1 and RAPTOR1B in the cytosol and by phosphorylation of RAPTOR1B by SnRK1 alpha 1 in kinase assays. Moreover, changed levels of phosphorylation states of several chloroplastic proteins in the snrk1 alpha 1/alpha 2 mutant indicated an unexpected link to regulation of photosynthesis, the main energy source in plants.
The impact of collagen modifications by methylglyoxal on fibroblast function and the role in aging
(2016)
SUBJECTS/METHODS: The study included 5597 boys and 5479 girls aged 7-8 years of age. Socioeconomic status (SES) was defined in three categories: high, medium and low. RESULTS: Between 1966 and 2012, the mean values for height and BMI significantly increased in both sexes (P<0.001). The variation of these two parameters, however, showed a different pattern. Whereas the variation in Z-values for height remained unchanged in both sexes, the variation in BMI increased in boys (P<0.01) but not in girls. SES affected the variation in Z-BMI in 1978 in both sexes (P<0.001), whereas variation in Z-height between SES categories remained unchanged across all years of surveys in boys. Before the political transformation, significant regional differences were observed in the variances of Z-BMI (P<0.05) but not of Z-height. This pattern changed after the political transformation, when regional differences in variances of Z-BMI disappeared. CONCLUSIONS: It is concluded that the mean values and the variation of BMI are affected by a changing quality of life, whereas the variation in height is usually independent of living conditions.
Despite a long history of plate convergence at the western margin of the South American plate that has been ongoing since at least the Early Paleozoic, the southern Peruvian fore-arc displays little to no evidence of shortening. In the light of this observation, we assess the deformation history of the southern Peruvian fore-arc and its geodynamic implications. To accomplish this, we present a new structural and geo-thermochronological data set (zircon U-Pb, mica Ar-40/Ar-39, apatite and zircon fission-track and zircon (U-Th)/He analyses) for samples collected along a 400km long transect parallel to the trench. Our results show that the Mesoproterozoic gneissic basement was mainly at temperatures 350 degrees C since the Neoproterozoic and was later intruded by Jurassic volcanic arc plutons. Along the coast, a peculiar apatite fission-track age pattern, coupled with field observations and a synthesis of available geological maps, allows us to identify crustal-scale tilted blocks that span the coastal Peruvian fore-arc. These blocks, bounded by normal faults that are orthogonal to the trench, suggest post-60Ma trench-parallel extension that potentially accommodated oroclinal bending in this region. Block tilting is consistent with the observed and previously described switch in the location of sedimentary sources in the fore-arc basin. Our data set allows us to estimate the cumulative slip on these faults to be less than 2km and questions the large amount of trench-parallel extension suggested to have accommodated this bending.
Exosomes are small membrane vesicles released by different cell types, including hepatocytes, that play important roles in intercellular communication. We have previously demonstrated that hepatocyte-derived exosomes contain the synthetic machinery to form sphingosine-1-phosphate (S1P) in target hepatocytes resulting in proliferation and liver regeneration after ischemia/reperfusion (I/R) injury. We also demonstrated that the chemokine receptors, CXCR1 and CXCR2, regulate liver recovery and regeneration after I/R injury. In the current study, we sought to determine if the regulatory effects of CXCR1 and CXCR2 on liver recovery and regeneration might occur via altered release of hepatocyte exosomes. We found that hepatocyte release of exosomes was dependent upon CXCR1 and CXCR2. CXCR1-deficient hepatocytes produced fewer exosomes, whereas CXCR2-deficient hepatocytes produced more exosomes compared to their wild-type controls. In CXCR2-deficient hepatocytes, there was increased activity of neutral sphingomyelinase (Nsm) and intracellular ceramide. CXCR1-deficient hepatocytes had no alterations in Nsm activity or ceramide production. Interestingly, exosomes from CXCR1-deficient hepatocytes had no effect on hepatocyte proliferation, due to a lack of neutral ceramidase and sphingosine kinase. The data demonstrate that CXCR1 and CXCR2 regulate hepatocyte exosome release. The mechanism utilized by CXCR1 remains elusive, but CXCR2 appears to modulate Nsm activity and resultant production of ceramide to control exosome release. CXCR1 is required for packaging of enzymes into exosomes that mediate their hepatocyte proliferative effect.
Exosomes are small membrane vesicles released by different cell types, including hepatocytes, that play important roles in intercellular communication. We have previously demonstrated that hepatocyte-derived exosomes contain the synthetic machinery to form sphingosine-1-phosphate (S1P) in target hepatocytes resulting in proliferation and liver regeneration after ischemia/reperfusion (I/R) injury. We also demonstrated that the chemokine receptors, CXCR1 and CXCR2, regulate liver recovery and regeneration after I/R injury. In the current study, we sought to determine if the regulatory effects of CXCR1 and CXCR2 on liver recovery and regeneration might occur via altered release of hepatocyte exosomes. We found that hepatocyte release of exosomes was dependent upon CXCR1 and CXCR2. CXCR1-deficient hepatocytes produced fewer exosomes, whereas CXCR2-deficient hepatocytes produced more exosomes compared to their wild-type controls. In CXCR2-deficient hepatocytes, there was increased activity of neutral sphingomyelinase (Nsm) and intracellular ceramide. CXCR1-deficient hepatocytes had no alterations in Nsm activity or ceramide production. Interestingly, exosomes from CXCR1-deficient hepatocytes had no effect on hepatocyte proliferation, due to a lack of neutral ceramidase and sphingosine kinase. The data demonstrate that CXCR1 and CXCR2 regulate hepatocyte exosome release. The mechanism utilized by CXCR1 remains elusive, but CXCR2 appears to modulate Nsm activity and resultant production of ceramide to control exosome release. CXCR1 is required for packaging of enzymes into exosomes that mediate their hepatocyte proliferative effect.