<?xml version="1.0" encoding="UTF-8"?>
<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns="http://purl.org/rss/1.0/" xmlns:dc="http://purl.org/dc/elements/1.1/">
  <channel rdf:about="https://scholar.dgist.ac.kr/handle/20.500.11750/265">
    <title>Repository Community: null</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/265</link>
    <description />
    <items>
      <rdf:Seq>
        <rdf:li rdf:resource="https://scholar.dgist.ac.kr/handle/20.500.11750/60615" />
        <rdf:li rdf:resource="https://scholar.dgist.ac.kr/handle/20.500.11750/60598" />
        <rdf:li rdf:resource="https://scholar.dgist.ac.kr/handle/20.500.11750/60579" />
        <rdf:li rdf:resource="https://scholar.dgist.ac.kr/handle/20.500.11750/60570" />
      </rdf:Seq>
    </items>
    <dc:date>2026-08-19T22:01:49Z</dc:date>
  </channel>
  <item rdf:about="https://scholar.dgist.ac.kr/handle/20.500.11750/60615">
    <title>The hippocampal CA3 area implements sequence learning of discontinuous episodes</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/60615</link>
    <description>Title: The hippocampal CA3 area implements sequence learning of discontinuous episodes
Author(s): Eom, Kisang; Kim, Yujin; Lee, Hyoung-Ro; Lee, Yolguk; Han, Young-Eun; Shin, Jiwoo; Lee, Jae Sung; Hyun, Jung Ho; Park, Alan J.; Lee, Suk-Ho
Abstract: Sequence learning requires linking memories of adjacent events by sharing ensemble cells. It remains unclear how the hippocampal CA3 links non-overlapping memory representations in sequence learning. High frequency mossy fiber inputs to a CA3 pyramidal cell downregulate Kv1.2 in distal apical dendrites to enhance its voltage response to perforant pathway inputs, and the high excitability is restored by subsequent perforant pathway inputs. Consistent with this notion, we found that CA3 ensemble cells activated by a novel context display high excitability, and their high excitability state is restored by re-activation during the second visit to a similar but distinct context. Computational modeling suggests that this bi-directional excitability regulation enables ordered association of orthogonal neuronal ensembles representing sequential events. Supporting this, CA3-specific Kcna2 + /- mice, which lack synaptic regulation of excitability, exhibited impaired sequence learning. These findings reveal the synaptic mechanisms by which the CA3 network encodes sequential memories.</description>
    <dc:date>2026-04-30T15:00:00Z</dc:date>
  </item>
  <item rdf:about="https://scholar.dgist.ac.kr/handle/20.500.11750/60598">
    <title>Loss of astrocytic Bmal1 promotes blood-brain barrier disruption and synaptic dysfunction during systemic inflammation</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/60598</link>
    <description>Title: Loss of astrocytic Bmal1 promotes blood-brain barrier disruption and synaptic dysfunction during systemic inflammation
Author(s): Lee, Changjun; Lee, Yelin; Jeong, Woo Chan; Hwang, Inhwa; Bae, Harin; Shim, Do-Wan; Jung, Hyeji; Um, Ji Won; Yu, Je-Wook
Abstract: Circadian rhythm disruption has been associated with the exaggerated inflammatory responses in peripheral tissues; however, its impact on neuroinflammation and blood-brain barrier (BBB) integrity remains unclear. Here, we identify the astrocytic circadian clock as a key regulator of BBB homeostasis during systemic inflammation. In a mouse model, circadian rhythm disruption for three weeks markedly increased BBB permeability in male mice, as evidenced by Evans blue leakage and myeloid cell infiltration into the brain parenchyma following lipopolysaccharide (LPS) challenge. Transcriptomic analyses using public datasets revealed that astrocytes exhibit the highest expression of core circadian clock genes among brain cell types. Accordingly, we generated tamoxifen-inducible, astrocyte-specific Bmal1-knockout (KO) mice. Deletion of Bmal1 in astrocytes significantly enhanced BBB leakage, astrogliosis and pericyte loss after LPS administration. Mechanistically, Bmal1-deficient astrocytes produced elevated levels of the chemokine CXCL5, which promoted CXCR2-dependent neutrophil recruitment into the brain. Pharmacological blockade of CXCR2 with SB225002 restored pericyte coverage and attenuated BBB disruption in astrocytic Bmal1 KO mice. Functionally, these mice exhibited impaired excitatory synaptic transmission following systemic inflammation, suggesting that astrocytic Bmal1 loss compromises neurovascular and synaptic integrity. Taken together, our findings demonstrate that astrocytic Bmal1 maintains BBB integrity and synaptic stability under inflammatory stress. This work also highlights astrocyte-intrinsic circadian regulation as a critical mechanism linking chemokine production to neurovascular vulnerability.</description>
    <dc:date>2026-04-30T15:00:00Z</dc:date>
  </item>
  <item rdf:about="https://scholar.dgist.ac.kr/handle/20.500.11750/60579">
    <title>hPMCA2w/b 유전자가 탑재된 벡터의 우울증 또는 불안 치료 용도</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/60579</link>
    <description>Title: hPMCA2w/b 유전자가 탑재된 벡터의 우울증 또는 불안 치료 용도
Author(s): 이효상
Abstract: hPMCA2w/b 유전자가 탑재된 벡터의 우울증 또는 불안 치료 용도에 관한 것으로, 본 발명에 따른 벡터 및 hPMCA2w/b 유전자가 도입된 뇌세포는 불안장애 및 우울증의 치료 효능이 우수하다.</description>
  </item>
  <item rdf:about="https://scholar.dgist.ac.kr/handle/20.500.11750/60570">
    <title>Gpr151 유전자의 5&amp;apos;UTR 또는 이의 변이체를 이용한 신경 손상의 치료</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/60570</link>
    <description>Title: Gpr151 유전자의 5&amp;apos;UTR 또는 이의 변이체를 이용한 신경 손상의 치료
Author(s): 이진영; 조용철; 전예원; 이봄; 신정은
Abstract: Disclosed is a composition for treating a neurological disease caused by nerve injury, including an isolated polynucleotide of a 5′-untranslated region (5′UTR) of a Gpr151 gene or a variant thereof. Also disclosed are a novel variant polynucleotide of 5′UTR of a Gpr151 gene and a vector including the polynucleo</description>
  </item>
</rdf:RDF>

