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    <title>DSpace community: 解剖學暨細胞生物學科暨研究所</title>
    <link>http://ntur.lib.ntu.edu.tw/handle/246246/16067</link>
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  <item rdf:about="http://ntur.lib.ntu.edu.tw/handle/246246/94553">
    <title>Neonates of Drug-Abusing Mothers: Experiences in a Medical Center in Northern Taiwan</title>
    <link>http://ntur.lib.ntu.edu.tw/handle/246246/94553</link>
    <description>title: Neonates of Drug-Abusing Mothers: Experiences in a Medical Center in Northern Taiwan abstract: Background: The aim of this study was to explore the patterns of drug abuse in pregnant women and the health problems of infants born to such women in northern Taiwan. Materials and Methods: From January 1990 through October 2005, the records of all neonates born at Mackay Memorial Hospital to mothers who had abused drugs during their pregnancies were reviewed. Results: Of the 37 neonates exposed prenatally to illicit drugs, 81% (30/37) developed neonatal abstinence syndrome. Withdrawal symptoms occurred in most infants within 72 hours of birth. The most common sign was tachypnea which required oxygen therapy. Other signs and symptoms included neurologic abnormalities ( tremors and irritability) and gastrointestinal dysfunction ( diarrhea, vomiting, and poor feeding). The course of the syndrome in the neonates correlated with the timing of the mother's last dose of the drug. Heroin was the most commonly abused drug during the most recent 5 years. Most of the infants were lost to follow up . Conclusions: In neonates with unexplained excitatory nervous and neuromuscular symptoms, neonatal withdrawal syndrome should be considered. A high index of suggestion and detailed maternal history are crucial for early detection and treatment.
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  <item rdf:about="http://ntur.lib.ntu.edu.tw/handle/246246/94552">
    <title>Differential Effects of Chronic Amphetamine and Baclofen Administration on Camp Levels and Phosphorylation of Creb in Distinct Brain Regions of Wild Type and Monoamine Oxidase B-Deficient Mice</title>
    <link>http://ntur.lib.ntu.edu.tw/handle/246246/94552</link>
    <description>title: Differential Effects of Chronic Amphetamine and Baclofen Administration on Camp Levels and Phosphorylation of Creb in Distinct Brain Regions of Wild Type and Monoamine Oxidase B-Deficient Mice abstract: Roles of GABA(B) transmission were explored in the action of amphetamine (Amph) on the brain. Adult male wild type (WT) and monoamine oxidase B- knocked out (MAOBKO) mice received i .p. injections of saline, d-Amph (5 mg/kg), plus baclofen ( GABAB receptor agonist, 10 mg/kg), or baclofen and Amph, twice daily for 3 days and single treatments on day 4, followed by immuno-cyclic-AMP (cAMP) and immunoblotting assays on the brain tissue. The WT mice responded with higher levels of behavioral responses than the KO to the daily Amph injection; however, baclofen blocked the Amph- induced behavioral hyperactivity of both WIT and KO mice. After the last treatment, levels of cAMP and phosphorylated (p) cyclic-AMP response element binding protein (CREB) were up-regulated in the striatum and somatosensory cortex of Amph-treated WT mice, while similar to the saline- controls in the baclofen+Amph-treated group, indicating the blockade by baclofen to Amph. Baclofen similarly suppressed the Amph- induced increases in pCREB levels of WIT hippocampus and amygdala, and decreases of olfactory bulb and thalamus. For MAOBKO mice, baclofen hindered the Amph-generated increases in motor cortical cAMP and pCREB, and amygdaloid pCREB, and the decrease in olfactory bulb pCREB, whereas did not affect the Amph-raised hippocampal pCREB. Furthermore, the levels of CREB were variably modified in distinct regions by the drug exposures. The data reveal that the GABA(B)-mediated intracellular signaling differentially participates in mechanisms underlying Amph perturbation to various regions , and may thereby contribute explanations to the behavioral consequences. Moreover, MAOB is region-dependently involved in responses of the brain to Amph and baclofen, supporting interactions between GABA and monoamines.
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  <item rdf:about="http://ntur.lib.ntu.edu.tw/handle/246246/94549">
    <title>Efns Guidelines on the Use of Skin Biopsy in the Diagnosis of Peripheral Neuropathy</title>
    <link>http://ntur.lib.ntu.edu.tw/handle/246246/94549</link>
    <description>title: Efns Guidelines on the Use of Skin Biopsy in the Diagnosis of Peripheral Neuropathy</description>
  </item>
  <item rdf:about="http://ntur.lib.ntu.edu.tw/handle/246246/94548">
    <title>C2gnt-M Is Downregulated in Colorectal Cancer and Its Re-Expression Causes Growth Inhibition of Colon Cancer Cells</title>
    <link>http://ntur.lib.ntu.edu.tw/handle/246246/94548</link>
    <description>title: C2gnt-M Is Downregulated in Colorectal Cancer and Its Re-Expression Causes Growth Inhibition of Colon Cancer Cells abstract: Changes in carbohydrates on the cell surface are associated with tumor malignancy. The mucin-type core 2 beta-1,6- N- acetylglucosaminyltransferase (C2GnT-M) is highly expressed in the gastrointestinal tract and catalyses the formation of core 2, core 4, and blood group I branches on O-glycans. In the present study, we evaluated the role of C2GnT-M in colorectal cancer. C2GnT-M downexpression was observed in 73 .6% of the primary tumors from colorectal cancer patients ( 39 of 53) analysed by cancer pro. ling array. Consistently, the majority of colon cancer cell lines and primary colon tumors expressed lower levels of C2GnT-M than did normal colon tissues by RT-PCR. HCT116 cells stably transfected with C2GnT-M inhibited expression of the core 1 structure, Gal beta 1,3GalNAc alpha 1-Ser/Thr, on the cell surface. Moreover, C2GnT-M expression suppressed cell adhesion, motility, and invasion as well as colony formation ability. The growth of C2GnT-M-transfected HCT116 and SW 480 cells was dramatically suppressed, and the cell death induced by C2 GnT-M was demonstrated by an increase in the annexin V- positive cells. Interestingly, C2GnT-M inhibited cell adhesion to collagen IV and fibronectin, and decreased tyrosine phosphorylation of paxillin, indicating that the changes in cancer behavior may be partly mediated by integrin-signaling pathways. Tumor growth in vivo was also significantly suppressed by C2GnT-M in the xenografts of nude mice. These results demonstrate that C2GnT-M is frequently downregulated in colorectal cancer and suppresses colon cancer cell growth.
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