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    <link>http://hdl.handle.net/2440/1091</link>
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    <pubDate>Mon, 20 May 2013 15:55:53 GMT</pubDate>
    <dc:date>2013-05-20T15:55:53Z</dc:date>
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      <title>Roles of EGF family of growth factors in growth: overview of their roles in postnatal growth and development</title>
      <link>http://hdl.handle.net/2440/77597</link>
      <description>Title: Roles of EGF family of growth factors in growth: overview of their roles in postnatal growth and development
Author: Xian, Cory J.; Shandala, Tetyana
Abstract: Ligands of the epidermal growth factor receptor (EGF-R), known to be important for supporting embryonic tissue development particularly in the gut and brain, have also been implicated in regulating postnatal somatic growth. While optimal levels of both milk-borne and endogenous EGF-R ligands are important for supporting postnatal somatic growth through regulating gastrointestinal growth and maturation, supra-physiological levels of EGF-R ligands can cause retarded and disproportionate growth and alter body composition as they increase growth of epithelial tissues but decrease masses of muscle, fat, and bone. EGF-R ligands can exert influence on growth indirectly via regulating levels of insulin-like growth factor (IGF-I) and its binding proteins (IGFBPs); EGFR ligands can also directly regulate bone growth and modeling, as they can enhance proliferation but suppress maturation of growth plate chondrocytes (for building a calcified cartilage scaffold for bone deposition) and osteoblasts (for depositing bone matrix), and promote formation and function of osteoclasts (for resorption of calcified cartilage or bone). In addition, EGF-R ligands, in particular amphiregulin, can themselves be regulated by parathyroid hormone (PTH), an important regulatory factor in bone modeling and remodeling. Finally, EGF-R ligands can regulate bone homeostasis by regulating pool of progenitor cells in the bone marrow through promoting their proliferation but suppressing differentiation of bone marrow mesenchymal stem cells.</description>
      <pubDate>Sat, 31 Dec 2011 13:30:00 GMT</pubDate>
      <guid isPermaLink="false">http://hdl.handle.net/2440/77597</guid>
      <dc:date>2011-12-31T13:30:00Z</dc:date>
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    <item>
      <title>Inhibition of CXCR2 profoundly suppresses inflammation-driven and spontaneous tumorigenesis</title>
      <link>http://hdl.handle.net/2440/77376</link>
      <description>Title: Inhibition of CXCR2 profoundly suppresses inflammation-driven and spontaneous tumorigenesis
Author: Jamieson, Thomas; Clarke, Mairi; Steele, Colin W.; Samuel, Michael Susithiran; Neumann, Jens; Jung, Andreas; Huels, David; Olson, Michael; Das, Sudipto; Nibbs, Robert J. B.; Sansom, Owen J.</description>
      <pubDate>Sat, 31 Dec 2011 13:30:00 GMT</pubDate>
      <guid isPermaLink="false">http://hdl.handle.net/2440/77376</guid>
      <dc:date>2011-12-31T13:30:00Z</dc:date>
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    <item>
      <title>Mutations in DEPDC5 cause familial focal epilepsy with variable foci</title>
      <link>http://hdl.handle.net/2440/77257</link>
      <description>Title: Mutations in DEPDC5 cause familial focal epilepsy with variable foci
Author: Dibbens, Leanne Michelle;...; Hughes, James Nicholas; Bellows, Susannah T.;...; Corbett, Mark Adam; Gardner, Alison E.;...; Mulley, John Charles; Dubeau, Francois;...; Thomas, Paul Quinton; Gécz, Jozef; ... et al.</description>
      <pubDate>Mon, 31 Dec 2012 13:30:00 GMT</pubDate>
      <guid isPermaLink="false">http://hdl.handle.net/2440/77257</guid>
      <dc:date>2012-12-31T13:30:00Z</dc:date>
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    <item>
      <title>Phthalates and perfluorooctanesulfonic acid in human amniotic fluid: temporal trends and timing of amniocentesis in pregnancy</title>
      <link>http://hdl.handle.net/2440/77218</link>
      <description>Title: Phthalates and perfluorooctanesulfonic acid in human amniotic fluid: temporal trends and timing of amniocentesis in pregnancy
Author: Jensen, Morten Søndergaard; Nørgaard-Pedersen, Bent; Toft, Gunnar; Hougaard, David M.; Bonde, Jens Peter; Cohen, Arieh; Thulstrup, Ane Marie; Ivell, Richard John; Anand Ivell, Ravinder Jit Kaur; Lindh, Christian H.; Jönsson, Bo A. G.
Abstract: BACKGROUND: Measures of prenatal environmental exposures are important, and amniotic fluid levels may directly reflect fetal exposures during hypothesized windows of vulnerability.    OBJECTIVES: We aimed to detect various phthalate metabolites and perfluorooctanesulfonic acid (PFOS) in human amniotic fluid, to study temporal exposure trends, and to estimate potential associations with gestational week of amniocentesis and maternal age and parity at amniocentesis. METHODS: We studied 300 randomly selected second-trimester amniotic fluid samples from a Danish pregnancy-screening biobank covering 1980 through 1996. We used only samples from male offspring pregnancies. We assayed the environmental pollutants by liquid chromatography/triple quadrupole mass spectrometry and analyzed data using generalized linear regression models. RESULTS: We detected the di(2-ethylhexyl) phthalate (DEHP) metabolite mono(2-ethyl-5-carboxypentyl) phthalate (5cx-MEPP) at a median concentration of 0.27 ng/mL [interquartile range (IQR): 0.20–0.37 ng/mL], the diisononyl phthalate (DiNP) metabolite mono(4-methyl-7-carboxyheptyl) phthalate (7cx-MMeHP) at 0.07 ng/mL (IQR: 0.05–0.11 ng/mL), and PFOS at 1.1 ng/mL (IQR: 0.66–1.60 ng/mL). An increase of 1 calendar year was associated with 3.5% lower [95% confidence interval (CI): –4.8%, –2.1%] 5cx-MEPP levels and with 7.1% higher (95% CI: 5.3%, 9.0%) 7cx-MMeHP levels. For each later gestational week of amniocentesis, 5cx-MEPP was 9.9% higher (95% CI: 4.8%, 15.2%), 7cx-MMeHP was 8.6% higher (95: CI: 2.7%, 14.9%), and PFOS was 9.4% higher (95: CI: 3.3%, 15.9%). We observed no associations with maternal age or parity.    CONCLUSIONS: Measured metabolite levels appeared to parallel decreasing DEHP exposure and increasing DiNP exposure during the study period. The environmental pollutant levels were positively associated with later gestational age at amniocentesis during pregnancy weeks 12–22.</description>
      <pubDate>Sat, 31 Dec 2011 13:30:00 GMT</pubDate>
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      <dc:date>2011-12-31T13:30:00Z</dc:date>
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