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    <title>DSpace community: 醫學院附設醫院</title>
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        <rdf:li resource="http://ntur.lib.ntu.edu.tw/handle/246246/171931" />
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  <item rdf:about="http://ntur.lib.ntu.edu.tw/handle/246246/171931">
    <title>A Planning and Navigation System for Neurosurgery</title>
    <link>http://ntur.lib.ntu.edu.tw/handle/246246/171931</link>
    <description>title: A Planning and Navigation System for Neurosurgery</description>
  </item>
  <item rdf:about="http://ntur.lib.ntu.edu.tw/handle/246246/171930">
    <title>Forkhead Proteins Are Critical for Bone Morphogenetic Protein-2 Regulation and Anti-Tumor Activity of Resveratrol</title>
    <link>http://ntur.lib.ntu.edu.tw/handle/246246/171930</link>
    <description>title: Forkhead Proteins Are Critical for Bone Morphogenetic Protein-2 Regulation and Anti-Tumor Activity of Resveratrol abstract: Osteoporosis is a major public health problem and the most obvious preventive strategy, hormone replacement therapy, has lost favor due to recent findings of the Women's Health Initiative regarding increased risks of breast cancer and cardiovascular disease. Resveratrol, a naturally occurring compound possessing estrogenic activity, is thought to have considerable potential for therapy of osteoporosis. In the present study, resveratrol was found to exhibit bone- protective effects equivalent to those exerted by hormone replacement therapy and decrease the risk of breast cancer in the in vivo and in vitro models. Forkhead proteins were found to be essential for both effects of resveratrol. The bone-protective effect was attributable to induction of bone morphogenetic protein-2 through Src kinase-dependent estrogen receptor activation and FOXA1 is required for resveratrol-induced estrogen receptor-dependent bone morphogenetic protein-2 expression. The tumor-suppressive effects of resveratrol were the consequence of Akt inactivation-mediated FOXO3a nuclear accumulation and activation. Resveratrol is therefore anticipated to be highly effective in management of postmenopausal osteoporosis without an increased risk of breast cancer.
&lt;br&gt;</description>
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  <item rdf:about="http://ntur.lib.ntu.edu.tw/handle/246246/171929">
    <title>Knockdown of Contactin-1 Expression Suppresses Invasion and Metastasis of Lung Adenocarcinoma</title>
    <link>http://ntur.lib.ntu.edu.tw/handle/246246/171929</link>
    <description>title: Knockdown of Contactin-1 Expression Suppresses Invasion and Metastasis of Lung Adenocarcinoma abstract: Numerous genetic changes are associated with cancer cell metastasis and invasion. In search for key regulators of invasion and metastasis, a panel of lung cancer cell lines with different invasive ability was screened. The gene for contactin-1 was found to play an essential role in tumor invasion and metastasis. Suppression of contactin-1 expression abolished the ability of lung adenocarcinoma cells to invade Matrigel in vitro as well as the polymerization of filamentous-actin and the formation of focal adhesion structures. Furthermore, knockdown of contactin-1 resulted in extensive inhibition of tumor metastasis and in increased survival in an animal model. RhoA but not Cdc42 or Rac1 was found to serve a critical role in contactin-1-mediated invasion and metastasis. Contactin-1-specific RNA interference resulted in loss of metastatic and invasive capacity in both in vitro and in vivo models. This loss was overturned by constitutive expression of the active form of RhoA. Contactin-1 was differentially expressed in tumor tissues, and its expression correlated with tumor stage , lymph node metastasis, and patient survival. Contactin-1 is proposed to function importantly in the invasion and metastasis of lung adenocarcinoma cells via RhoA-mediated mechanisms.
&lt;br&gt;</description>
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  <item rdf:about="http://ntur.lib.ntu.edu.tw/handle/246246/171928">
    <title>Use of Extracorporeal Membrane Oxygenation to Rescue a Child with Acute Respiratory Distress Syndrome</title>
    <link>http://ntur.lib.ntu.edu.tw/handle/246246/171928</link>
    <description>title: Use of Extracorporeal Membrane Oxygenation to Rescue a Child with Acute Respiratory Distress Syndrome abstract: Acute respiratory distress syndrome (ARDS) carries a high mortality of about 60%. The results of conventional treatments for ARDS are poor. We report the use of extracorporeal membrane oxygenation (ECMO) to rescue a child with ARDS. The patient, a 7-year-old boy, underwent a Ross procedure and mitral valvuloplasty because of severe aortic and mild mitral regurgitation.;ARDS due to massive transfusion and prolonged cardiopulmonary by-pass developed in the early postoperative period. Hypoxemia persisted despite conventional treatments, including pressure- controlled ventilation and high-frequency ventilation. Finally, venovenous ECMO was used to rescue the patient. With ECMO support, gas exchange was well maintained with a lower ventilator setting, and ventilator-induced Lung injuries were avoided. ECMO was used for 183 hours, at which point the boy was weaned without complications. His recovery was uneventful. At the latest followup, 6 months after the operation, he was in New York Heart Association function class I and had no complaints of lung disease. This case suggests that venovenous ECMO can be a rescue method for patients with ARDS that is refractory to conventional treatments.
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