台湾人女性とベリーダンス : 変容する女性らしさに関する人類学的研究

早大学位記番号:新6518早稲田大

Towards End-to-End Embodied Decision Making via Multi-modal Large Language Model: Explorations with GPT4-Vision and Beyond

In this study, we explore the potential of Multimodal Large Language Models (MLLMs) in improving embodied decision-making processes for agents. While Large Language Models (LLMs) have been widely used due to their advanced reasoning skills and vast world knowledge, MLLMs like GPT4-Vision offer enhanced visual understanding and reasoning capabilities. We investigate whether state-of-the-art MLLMs can handle embodied decision-making in an end-to-end manner and whether collaborations between LLMs and MLLMs can enhance decision-making. To address these questions, we introduce a new benchmark called PCA-EVAL, which evaluates embodied decision-making from the perspectives of Perception, Cognition, and Action. Additionally, we propose HOLMES, a multi-agent cooperation framework that allows LLMs to leverage MLLMs and APIs to gather multimodal information for informed decision-making. We compare end-to-end embodied decision-making and HOLMES on our benchmark and find that the GPT4-Vision model demonstrates strong end-to-end embodied decision-making abilities, outperforming GPT4-HOLMES in terms of average decision accuracy (+3%). However, this performance is exclusive to the latest GPT4-Vision model, surpassing the open-source state-of-the-art MLLM by 26%. Our results indicate that powerful MLLMs like GPT4-Vision hold promise for decision-making in embodied agents, offering new avenues for MLLM research. Code and data are open at https://github.com/pkunlp-icler/PCA-EVAL/.Comment: FMDM@NeurIPS2023, Code and data: https://github.com/pkunlp-icler/PCA-EVAL

Mutation and Lineage Analysis of DNMT3A in BCR-ABL1-negative Chronic Myeloproliferative Neoplasms

SummaryIn addition to the JAK2 V617F mutation, somatic mutation in DNMT3A has been described in BCL-ABL1-negative myeloproliferative neoplasms (MPNs). We have screened for DNMT3A exon 23 mutations in 130 adult Taiwanese patients with chronic phase myeloproliferative neoplasms. Only one somatic DNMT3A R882H mutation was identified in one JAK2 V617F mutation-positive essential thrombocythemia patient (1/91, 1%). Both mutations were detected in the CD34+-, CD19+-, peripheral blood mononuclear cell- and granulocyte-enriched fractions, but were not detected in the CD3+-enriched fraction by lineage analysis. Our findings suggest that DNMT3A mutation is not prevalent in MPNs, and further study is needed to clarify its role in the molecular pathogenesis of myeloproliferative neoplasms

Learning to recommend descriptive tags for questions in social forums

10.1145/2559157ACM Transactions on Information Systems321-ATIS

Structural insights into Ca2+-activated long-range allosteric channel gating of RyR1

Ryanodine receptors (RyRs) are a class of giant ion channels with molecular mass over 2.2 mega-Daltons. These channels mediate calcium signaling in a variety of cells. Since more than 80% of the RyR protein is folded into the cytoplasmic assembly and the remaining residues form the transmembrane domain, it has been hypothesized that the activation and regulation of RyR channels occur through an as yet uncharacterized long-range allosteric mechanism. Here we report the characterization of a Ca2+-activated open-state RyR1 structure by cryo-electron microscopy. The structure has an overall resolution of 4.9 angstrom and a resolution of 4.2 angstrom for the core region. In comparison with the previously determined apo/closed-state structure, we observed long-range allosteric gating of the channel upon Ca2+ activation. In-depth structural analyses elucidated a novel channel-gating mechanism and a novel ion selectivity mechanism of RyR1. Our work not only provides structural insights into the molecular mechanisms of channel gating and regulation of RyRs, but also sheds light on structural basis for channel-gating and ion selectivity mechanisms for the six-transmembrane-helix cation channel family.Strategic Priority Research Program of Chinese Academy of Sciences [XDB08030202]; National Basic Research Program (973 Program); Ministry of Science & Technology of China [2012CB917200, 2014CB910700]; National Natural Science Foundation of China [31270768]; Ministry of Education of China (111 Program China)SCI(E)PubMed中国科技核心期刊(ISTIC)[email protected]; [email protected]

DEVELOPMENTAL EXPOSURE TO DIESEL EXHAUST CAUSES AUTISM-LIKE BEHAVIORAL, MOLECULAR, AND CORTICAL STRUCTURAL ALTERATIONS.

Thesis (Ph.D.)--University of Washington, 2018Escalating prevalence of autism spectrum disorders (ASD) in recent decades has triggered increasing efforts in understanding the role played by environmental risk factors as a way to address this widespread public health concern. Several epidemiological studies show associations between developmental exposure to traffic-related air pollution and increased ASD risk. The purpose of this project was to elucidate the neurotoxic mechanisms of developmental exposure to traffic-related air pollution in mice. A series of experiments were performed to determine whether developmental diesel exhaust (DE) exposure induces ASD-related behaviors, and whether the neuroinflammatory pathway leading to dysregulation of reelin expression was affected. C57Bl/6J mice were exposed from GD0 to PND21 to 250-300 g/m3 DE or filtered air (FA) as control. DE-exposed mice exhibited deficits in all three of the hallmark categories of ASD behavior: disrupted social interaction in the reciprocal interaction test and social preference test, disrupted social olfactory and vocal communication, and increased repetitive behavior. In brains of DE-exposed mice, increased levels of interleukin-6, increased phosphorylation of STAT3, increased expression of DNMT1, and decreased expression of reelin were found. Furthermore, cortical lamina organization was examined with immunohistochemistry staining, and subtle but significant differences in the distribution pattern of neurons expressing layer-specific markers were found. Additionally, increased PAX6, Tbr2, and Tbr1 mRNA levels were found in brains of neonatal DE- exposed mice, suggesting early promotion of the neurogenic pathway over preservation of neural progenitor cells’ self-renewal ability, which is supported by our finding of decreased adult neurogenesis in the hippocampal dentate gyrus of PND60 DE- exposed mice. Overall, these studies show that developmental DE exposure, taken as a measure of traffic-related air pollution, causes behavioral, biochemical/molecular and structural changes that resemble those present in ASD