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  <channel rdf:about="https://scholar.dgist.ac.kr/handle/20.500.11750/290">
    <title>Repository Collection: null</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/290</link>
    <description />
    <items>
      <rdf:Seq>
        <rdf:li rdf:resource="https://scholar.dgist.ac.kr/handle/20.500.11750/59011" />
        <rdf:li rdf:resource="https://scholar.dgist.ac.kr/handle/20.500.11750/47129" />
        <rdf:li rdf:resource="https://scholar.dgist.ac.kr/handle/20.500.11750/47052" />
        <rdf:li rdf:resource="https://scholar.dgist.ac.kr/handle/20.500.11750/47048" />
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    <dc:date>2026-04-04T17:06:32Z</dc:date>
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  <item rdf:about="https://scholar.dgist.ac.kr/handle/20.500.11750/59011">
    <title>Metabolomic profiling in blood of pancreatic cancer patients</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/59011</link>
    <description>Title: Metabolomic profiling in blood of pancreatic cancer patients
Author(s): Kim, Hyojeong; Kim, Dong-uk; Choe, Sangmin; Lee, SeungHun; Kim, Eun-Kyoung; Park, Seokjae
Abstract: Background
Pancreatic cancer has a poor prognosis. One of the reasons is that it is difficult to diagnose early. There has been abundant evidence that malignant cells rewire their metabolism to survive and proliferate. This study examined differentia of metabolomic profiling between patients with advanced pancreatic cancers and volunteers without ones.
Methods
Ten patients and 10 volunteers who aged 20 years or older were enrolled between May and December 2015. The patients had been confirmed as pancreatic ductal adenocarcinoma cytologically or histologically. The volunteers were those who had examined abdomen CT during their health screenings and had no evidence suggesting pancreatic cancer. Blood plasma samples were derivatized and analyzed by gas chromatography mass spectrometry (GC-MS). GC-MS (Agilent 5975C MSD + 7890A GC) data produced by untargeted method were analyzed by statistical methods including principal Component Analyses (PCA).
Results
Lactic acid showed significantly high concentration with fold change of 3.23 in patients group (P ≤ 0.0001). 1,5-Anhydroglucitol was decreased with fold change of 2.94 in patients group (P ≤ 0.0001).
Conclusion
This study suggest that pancreatic cancer patients could have different metabolomic profiling from normal population. Further investigation is required for the development of early diagnosis as well exploration of potentially therapeutic target.</description>
    <dc:date>2017-07-26T15:00:00Z</dc:date>
  </item>
  <item rdf:about="https://scholar.dgist.ac.kr/handle/20.500.11750/47129">
    <title>Hypothalamic autophagy mediated by AMPK regulates food intake</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/47129</link>
    <description>Title: Hypothalamic autophagy mediated by AMPK regulates food intake
Author(s): Kim, Eun-Kyoung</description>
    <dc:date>2017-10-07T15:00:00Z</dc:date>
  </item>
  <item rdf:about="https://scholar.dgist.ac.kr/handle/20.500.11750/47052">
    <title>Roles of autophagy in palmitate-induced ER stress and apoptosis in hypothalamic neuronal cells</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/47052</link>
    <description>Title: Roles of autophagy in palmitate-induced ER stress and apoptosis in hypothalamic neuronal cells
Author(s): Lim, Yun; Kim, Eun-Kyoung
Abstract: Autophagy is a cellular process that degrades damaged organelles and aggregated proteins. Hypothalamic autophagy is important for regulation of food intake and energy expenditure. High-fat diet induces hypothalamic injury through endoplasmic reticulum (ER) stress and apoptosis in rodents. We demonstrate here that autophagy plays a role in protecting hypothalamic neuronal cells from ER stress-induced apoptosis. Treatment of palmitate induces ER stress and autophagy in hypothalamic neuronal cells, N41. However, prolonged treatment of palmitate impairs autophagy and increases apoptosis. When palmitate-induced autophagy is enhanced by rapamycin, an autophagy inducer, ER stress and apoptosis are decreased. On the other hand, treatment of bafilomycin, an autophagy inhibitor, increases ER stress and apoptosis. In addition, pretreatment of ER stress reducer to palmitate decreases both autophagy and apoptosis. Taken together, our results indicate that autophagy has a protective role in cellular homeostasis by regulating ER stress. Our study suggests that modulation of autophagy is a possible therapeutic strategy for metabolic disorders such as obesity and diabetes.</description>
    <dc:date>2017-11-12T15:00:00Z</dc:date>
  </item>
  <item rdf:about="https://scholar.dgist.ac.kr/handle/20.500.11750/47048">
    <title>Brain-derived insulin-expressing neurons in the paraventricular nucleus of the hypothalamus project to the median eminence</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/47048</link>
    <description>Title: Brain-derived insulin-expressing neurons in the paraventricular nucleus of the hypothalamus project to the median eminence
Author(s): Kim, Kyung Chan; Lee, Jae Meun; Jo, Jae Hyeon; Kim, Eun-Kyoung
Abstract: Although it had been considered that pancreatic β-cells are the major source of circulating hormonal insulin, the evidence has mounted that insulin can also be synthesized in the diverse brain regions including cerebral cortex, striatum, olfactory bulb, hippocampus, and hypothalamus. Our previous study showed that acute Wnt3a injection into the third ventricle (3V) upregulates insulin gene expression in the adult mouse hypothalamus. Nevertheless, little is known which hypothalamic regions are involved in insulin production and its release. In the present study, we found a novel neuronal population expressing brain-derived insulin (BDI) in the paraventricular nucleus of the hypothalamus (PVN) by using immunolabeling and in situ hybridization. PVN BDI-expressing neurons project their axon terminals into the external zone of the median eminence (ME). Interestingly, approximately 85% of PVN BDI-expressing neurons co-express corticotrophin-releasing hormone (CRH). Furthermore, these neurons co-transport BDI and CRH into the ME. Taken together, we first report that BDI is expressed in the PVN neurons projecting to the ME.</description>
    <dc:date>2017-11-14T15:00:00Z</dc:date>
  </item>
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