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    <title>Repository Community: null</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/131</link>
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        <rdf:li rdf:resource="https://scholar.dgist.ac.kr/handle/20.500.11750/61003" />
        <rdf:li rdf:resource="https://scholar.dgist.ac.kr/handle/20.500.11750/60905" />
        <rdf:li rdf:resource="https://scholar.dgist.ac.kr/handle/20.500.11750/60623" />
        <rdf:li rdf:resource="https://scholar.dgist.ac.kr/handle/20.500.11750/60385" />
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    <dc:date>2026-10-28T01:02:22Z</dc:date>
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  <item rdf:about="https://scholar.dgist.ac.kr/handle/20.500.11750/61003">
    <title>Thalamofrontal synaptic weakening underlies short-term memory deficits from adolescent NMDAR hypofunction</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/61003</link>
    <description>Title: Thalamofrontal synaptic weakening underlies short-term memory deficits from adolescent NMDAR hypofunction
Author(s): Yu, Jinseon; Choi, In Sun; Kim, Gyu Hyun; Bahn, Sangkyu; Kim, Jinmo; Bae, Sungwon; Lee, Taekwan; Choi, Joon Ho; Kwon, Jun Soo; Kim, Minah; Choi, Ji-Woong; Lee, Kea Joo; Rah, Jong-Cheol
Abstract: Thalamofrontal (TF) dysconnectivity is one of the most consistent circuit-level abnormalities reported in patients with schizophrenia and is linked to deficits in short-term memory (STM). However, the biological mechanisms underlying TF weakening remain unclear. Here, we show that repeated adolescent N-methyl-d-aspartate receptor (NMDAR) antagonism produces STM deficits by impairing TF synaptic transmission. In mice repeatedly exposed to ketamine, STM impairment coincided with reduced release probability and attenuated short-term depression at mediodorsal thalamus (MD) -&gt; dorsomedial prefrontal cortex (dmPFC) synapses, without detectable changes in corticocortical synaptic release probability, intrinsic excitability, or gross synaptic ultrastructure. These presynaptic deficits were accompanied by diminished direction-selective population coding in the dmPFC and impaired delayed alternation performance. Chemogenetically strengthening MD -&gt; dmPFC projections restored both neural selectivity and behavior. These findings identify a projection-specific presynaptic mechanism through which adolescent NMDAR hypofunction weakens TF communication and produces cognitive impairment, offering a biological explanation for clinically observed TF dysconnectivity and establishing TF synapses as a therapeutic target.</description>
    <dc:date>2026-08-31T15:00:00Z</dc:date>
  </item>
  <item rdf:about="https://scholar.dgist.ac.kr/handle/20.500.11750/60905">
    <title>Translational Profiling of Drd2-Expressing Populations Reveals Molecular Heterogeneity of Dentate Gyrus Mossy Cells along the Dorsoventral Axis</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/60905</link>
    <description>Title: Translational Profiling of Drd2-Expressing Populations Reveals Molecular Heterogeneity of Dentate Gyrus Mossy Cells along the Dorsoventral Axis
Author(s): Jeong, Minseok; Jang, Jin-Hyeok; Oh, Seo-Jin; Choi, Ji-Woong; Oh, Yong-Seok
Abstract: Hilar mossy cells (MCs) are crucial for integrating and propagating signals across the hippocampal dorsoventral axis, mediating cognitive and affective processing. While MCs exhibit profound dorsoventral differences in their projections, physiology, and behavioral roles, the molecular basis underlying this functional specialization remains largely unexplored. To address this gap, we used translating ribosome affinity purification (TRAP) in male mice to systematically compare the translatome of Drd2-expressing, MC-enriched populations along the dorsoventral axis. This analysis revealed distinct translational signatures with 1,442 genes enriched in dorsal and 1,337 genes in ventral Drd2-expressing, MC-enriched populations. Pathway analysis demonstrated significant functional segregation along the dorsoventral axis. The dorsal population is notably enriched for genes linked to neuronal connectivity and synaptic transmission, whereas the ventral counterpart shows enrichment in genes associated with energy metabolism and cellular maintenance. Specifically, we identified a subset of dorsal enriched genes, including neurotransmitter receptors, ion channels, and axon guidance regulators, contrasting with ventral enriched genes highly related to glucose/fatty acid metabolism, oxidative phosphorylation, and exocytosis. We further predicted distinct sets of upstream transcriptional regulators activated in each subpopulation, providing insights into the regulatory networks that may drive molecular divergence. Our findings provide a translatomic basis for the dorsoventral heterogeneity of Drd2-expressing neurons that include MCs, offering molecular signatures associated with their differential contributions to hippocampal function.</description>
    <dc:date>2026-06-30T15:00:00Z</dc:date>
  </item>
  <item rdf:about="https://scholar.dgist.ac.kr/handle/20.500.11750/60623">
    <title>Iterative Joint Detection and ORBGRAND for Massive Multi-User MIMO</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/60623</link>
    <description>Title: Iterative Joint Detection and ORBGRAND for Massive Multi-User MIMO
Author(s): Park, Hanyoung; Choi, Ji-Woong
Abstract: Multi-user multi-input multi-output (MU-MIMO) is a key enabler for next-generation wireless systems, but its performance is often limited by strong interference from inter-user channel correlations and the lack of decoding-aware detection strategies. To address this challenge, we propose a joint iterative detection and decoding algorithm that consists of detection, ordered reliability bits guessing random additive noise decoding (ORBGRAND), and hard/soft parallel interference cancellation (PIC) switching, in consideration of inter-user channel correlation and decoding failure. Simulation results demonstrate that the proposed scheme outperforms state-of-the-art baselines, providing a significantly improved block error rate (BLER). These results highlight the potential of the proposed method as an efficient and robust solution for coded MU-MIMO systems.</description>
    <dc:date>2025-12-31T15:00:00Z</dc:date>
  </item>
  <item rdf:about="https://scholar.dgist.ac.kr/handle/20.500.11750/60385">
    <title>복소 영역에서의 수신 파워와 위상을 이용한 통신 신호 탐지 시스템 및 그 방법</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/60385</link>
    <description>Title: 복소 영역에서의 수신 파워와 위상을 이용한 통신 신호 탐지 시스템 및 그 방법
Author(s): 오대건; 최지웅; 진우철
Abstract: 본 발명은 복소 영역에서의 수신 파워와 위상을 이용한 통신 신호 탐지 시스템 및 그 방법에 관한 것이다. 본 발명에 따르면, 복소 영역에서의 수신 파워와 위상을 이용한 통신 신호 탐지 시스템에 있어서, 복소 성분을 가지는 RF 신호를 수신하는 신호 수신부; 상기 수신된 RF 신호에 대해 푸리에 변환을 수행하는 변환부; 상기 변환된 RF 신호의 수신 파워를 산출하고, 기 설정된 임계값과 비교하는 비교부; 상기 산출된 수신 파워가 기 설정된 임계값보다 큰 경우 상기 변환된 RF 신호의 I 채널 성분과 Q 채널 성분의 위상 차이를 연산하는 연산부; 및 상기 I 채널 성분과 Q 채널 성분의 위상 차이가 기 지정된 범위에 포함되면 상기 RF 신호 내의 통신 신호를 탐지하는 탐지부를 포함한다. 본 발명에 따르면, 통신 신호를 탐지하는 탐지율은 유지하고, 노이즈에 의한 오탐지를 감소시킬 수 있다.</description>
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