93 research outputs found
Fear conditioning occludes late-phase long-term potentiation at thalamic input synapses onto the lateral amygdala in rat brain slices
No full textLate-phase long-term potentiation (L-LTP) of excitatory synaptic transmission at thalamic input synapses onto the lateral amygdala (T-LA synapses) has been proposed as a cellular substrate for long-term fear memory. This notion is evidenced primarily by previous reports in which the same pharmacological treatments block both T-LA L-LTP and the consolidation of fear memory. In this study, we report that fear conditioning occludes L-LTP at T-LA synapses in brain slices prepared after fear memory consolidation. L-LTP was restored either when synaptic depotentiation was induced prior to L-LTP induction in brain slices prepared from conditioned rats or when brain slices were prepared from conditioned rats that had been exposed to subsequent fear extinction, which is a behavior paradigm known to induce in vivo synaptic depotentiation at T-LA synapses. These results suggest that fear conditioning recruits L-LTP-like mechanisms that are reversible and saturable at T-LA synapses. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
Distributed human computation framework for linked data co-reference resolution
No full textDistributed Human Computation (DHC) is a technique used to solve computational problems by incorporating the collaborative effort of a large number of humans. It is also a solution to AI-complete problems such as natural language processing. The Semantic Web with its root in AI is envisioned to be a decentralised world-wide information space for sharing machine-readable data with minimal integration costs. There are many research problems in the Semantic Web that are considered as AI-complete problems. An example is co-reference resolution, which involves determining whether different URIs refer to the same entity. This is considered to be a significant hurdle to overcome in the realisation of large-scale Semantic Web applications. In this paper, we propose a framework for building a DHC system on top of the Linked Data Cloud to solve various computational problems. To demonstrate the concept, we are focusing on handling the co-reference resolution in the Semantic Web when integrating distributed datasets. The traditional way to solve this problem is to design machine-learning algorithms. However, they are often computationally expensive, error-prone and do not scale. We designed a DHC system named iamResearcher, which solves the scientific publication author identity co-reference problem when integrating distributed bibliographic datasets. In our system, we aggregated 6 million bibliographic data from various publication repositories. Users can sign up to the system to audit and align their own publications, thus solving the co-reference problem in a distributed manner. The aggregated results are published to the Linked Data Cloud
New insights into the regulation of leaf senescence in Arabidopsis
No full textPlants undergo developmental changes throughout their life history. Senescence, the final stage in the life history of a leaf, is an important and unique developmental process whereby plants relocate nutrients from leaves to other developing organs, such as seeds, stems, or roots. Recent attempts to answer fundamental questions about leaf senescence have employed a combination of new ideas and advanced technologies. As senescence is an integral part of a plant's life history that is linked to earlier developmental stages, age-associated leaf senescence may be analysed from a life history perspective. The successful utilization of multi-omics approaches has resolved the complicated process of leaf senescence, replacing a component-based view with a network-based molecular mechanism that acts in a spatial-temporal manner. Senescence and death are critical for fitness and are thus evolved characters. Recent efforts have begun to focus on understanding the evolutionary basis of the developmental process that incorporates age information and environmental signals into a plant's survival strategy. This review describes recent insights into the regulatory mechanisms of leaf senescence in terms of systems-level spatiotemporal changes, presenting them from the perspectives of life history strategy and evolution
© The Author(s) 2017. Published by Oxford University Press on behalf of the Society for Experimental Biology. All rights reserved4
COX-2 regulates the insulin-like growth factor I-induced potentiation of Zn2+-toxicity in primary cortical culture
No full textThe pretreatment of cultured cortical neurons with neurotrophic factors markedly potentiates the cytotoxicity induced by low concentrations of Zn2+ or excitotoxins. In the current study, we investigated the mechanism underlying the insulin-like growth factor-I (IGF-I)-induced Zn2+ toxicity potentiation. The pretreatment of primary cortical cultures for more than 12 h with 100 ng/ml of IGF-I increased the cytotoxicity induced by 80 muM Zn2+ by more than 2-fold. The IGF-I-enhanced cell death was blocked by the COX-2-specific inhibitors N-[2-(cyclohexyloxyl)-4-nitrophenyl]methane sulfonamide (NS-398; 10-100 muM) and 1-[(4-methylsulfonyl)phenyl]-3-trifluoro-methyl-5-[(4-fluoro)phenyl]pyrazole (SC58125; 10 muM) and by the antioxidant trolox (30 muM). In addition, it was observed that COX-2 expression was increased 12 to 24 h after IGF-I treatment. Preincubation of cortical cultures with IGF-I increased arachidonic acid (AA)-induced cytotoxicity, and AA increased Zn2+ toxicity, which suggested the involvement of COX activity in these cellular responses. Moreover, enhanced COX-2 activity led to a decrease in the cell's reducing power, as indicated by a gradual depletion of intracellular GSH. Cortical neurons pretreated with IGF-I and then Zn2+ showed consistently enhanced reactive oxygen species production, which was repressed by NS-398 and SC58125. Cortical neurons treated with Zn2+ and then AA displayed the increased ROS production, which was also suppressed by NS-398 and SC58125. These results suggest that COX-2 is an endogenous factor responsible for the IGF-I-induced potentiation of Zn2+ toxicity and that enhanced COX-2 activity leads to a decrease in the cell's reducing power and an increase in ROS accumulation in primary cortical cultures
Notch interferes with the scaffold function of JNK-interacting protein 1 to inhibit the JNK signaling pathway
No full textThe transmembrane protein Notch is cleaved by gamma-secretase to yield an active form, Notch intracellular domain (Notch-IC), in response to the binding of ligands, such as Jagged. Notch-IC contributes to the regulation of a variety of cellular events, including cell fate determination during embryonic development as well as cell growth, differentiation, and survival. We now show that Notch1-IC suppresses the scaffold activity of c-Jun N-terminal kinase (JNK)-interacting protein 1 (JIP1) in the JNK signaling pathway. Notch1-IC physically associated with the JNK binding domain of JlP1 and thereby interfered with the interaction between JlP1 and JNK. JlP1 mediated the activation of JNK1 induced by glucose deprivation in mouse embryonic fibroblasts, and ectopic expression of Notch1-IC inhibited JNK activation and apoptosis triggered by glucose deprivation. Taken together, these findings suggest that Notch1-IC negatively regulates the JNK pathway by disrupting the scaffold function of JIP1
Integration of a rehabilitation robotic system (KARES II) with human-friendly man-machine interaction units
No full textIn this paper, we report some important results of design and evaluation of a wheelchair-based robotic arm system, named as KARES II (KAIST Rehabilitation Engineering Service System II), which is newly developed for the disabled. KARES II is designed in consideration of surveyed necessary tasks for the target users ( that is, people with spinal cord injury). At first, we predefined twelve important tasks according to extensive interviews and questionnaires. Next, based on these tasks, all subsystems are designed, simulated and developed. A robotic arm with active compliance and intelligent visual servoing capability is developed by using cable-driven mechanism. Various kinds of human-robot interfaces are developed to provide broad range of services according to the levels of disability. Eye-mouse, shoulder/head interface, EMG signal-based control subsystems are used for this purpose. Besides, we describe the process of integration of our rehabilitation robotic system KARES II, and discuss about user trials. A mobile platform and a wheelchair platform are two main platforms in which various subsystems are installed. For a real-world application of KARES II system, we have performed user trials with six selected potential end-users ( with spinal cord injury).This work is fully supported by the Ministry of Science
and Technology of Korea as a part of Critical
Technology 21 Program on “Development of Intelligent
Human-Robot Interaction Technology.” We also
like to acknowledge various forms of support from Dr.
Byung-Sik Kim and his staff of National Rehabilitation
Center, Korea
High-Throughput and Computational Study of Leaf Senescence through a Phenomic Approach
No full textLeaf senescence is influenced by its life history, comprising a series of developmental and physiological experiences. Exploration of the biological principles underlying leaf lifespan and senescence requires a schema to trace leaf phenotypes, based on the interaction of genetic and environmental factors. We developed a new approach and concept that will facilitate systemic biological understanding of leaf lifespan and senescence, utilizing the phenome high-throughput investigator (PHI) with a single-leaf-basis phenotyping platform. Our pilot tests showed empirical evidence for the feasibility of PHI for quantitative measurement of leaf senescence responses and improved performance in order to dissect the progression of senescence triggered by different senescence-inducing factors as well as genetic mutations. Such an establishment enables new perspectives to be proposed, which will be challenged for enhancing our fundamental understanding on the complex process of leaf senescence. We further envision that integration of phenomic data with other multi-omics data obtained from transcriptomic, proteomic, and metabolic studies will enable us to address the underlying principles of senescence, passing through different layers of information from molecule to organism.
© 2017 Lyu, Baek, Jung, Chu, Nam, Kim and Lim. This is an open-access
article distributed under the terms of the Creative Commons Attribution License
(CC BY). The use, distribution or reproduction in other forums is permitted, provided
the original author(s) or licensor are credited and that the original publication in this
journal is cited, in accordance with accepted academic practice. No use, distribution
or reproduction is permitted which does not comply with these terms. © 2017 Lyu, Baek, Jung, Chu, Nam, Kim and Lim. This is an open-access
article distributed under the terms of the Creative Commons Attribution License
(CC BY). The use, distribution or reproduction in other forums is permitted, provided
the original author(s) or licensor are credited and that the original publication in this
journal is cited, in accordance with accepted academic practice. No use, distribution
or reproduction is permitted which does not comply with these terms.
© 2017 Lyu, Baek, Jung, Chu, Nam, Kim and Lim. This is an open-access
article distributed under the terms of the Creative Commons Attribution License
(CC BY). The use, distribution or reproduction in other forums is permitted, provided
the original author(s) or licensor are credited and that the original publication in this
journal is cited, in accordance with accepted academic practice. No use, distribution
or reproduction is permitted which does not comply with these terms.2
Rapid Disruption of Cellular Integrity of Zinc-treated Astroglia Is Regulated by p38 MAPK and Ca<sup>2＋</sup>-dependent Mechanisms
No full textExtracellular and intracellular glutathione protectts astrocytes from Zn2+-induced cell death
No full textFree Zn2+ is released in excess at excitatory synapses in pathological conditions including transient global and focal cerebral ischemia, which causes neuronal and glial cell death. In the current study, we explored the mechanism underlying Zn2+-induced cell death in primary cortical astroglial cultures. Chronic treatment with 30–35 µM Zn2+ led to the death of 70–95% of astrocytes within 18 h, preceded by Zn2+ influx. Extracellular glutathione (GSH; 100 µM) completely blocked the Zn2+ influx and Zn2+ toxicity. The Zn2+ toxicity was also inhibited when intracellular GSH was increased. Conversely, it was aggravated when intracellular GSH was depleted by buthionine sulfoximine (BSO). Consistently, the level of cellular GSH was notably decreased with a concurrent increase in oxidized GSH in Zn2+-treated astrocytes. These results suggest that the disruption of proper maintenance of thiol homeostasis is a mechanism underlying Zn2+ toxicity in primary cortical astrocytes.This study was supported by a grant (02-PJ1-PG3-21304-0011) of the Korea Health 21 R and D Project, Ministry of Health and Welfare, Republic of Korea for P-L Ha
JNK pathway is required for retinoic acid-induced neurite outgrowth of human neuroblastoma, SH-SY5Y
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