<?xml version="1.0" encoding="UTF-8"?>
<collection xmlns="http://www.loc.gov/MARC21/slim">
 <record>
  <leader>     caa a22        4500</leader>
  <controlfield tag="001">475787234</controlfield>
  <controlfield tag="003">CHVBK</controlfield>
  <controlfield tag="005">20180406123702.0</controlfield>
  <controlfield tag="007">cr unu---uuuuu</controlfield>
  <controlfield tag="008">170329e20001001xx      s     000 0 eng  </controlfield>
  <datafield tag="024" ind1="7" ind2="0">
   <subfield code="a">10.1007/s004310000587</subfield>
   <subfield code="2">doi</subfield>
  </datafield>
  <datafield tag="035" ind1=" " ind2=" ">
   <subfield code="a">(NATIONALLICENCE)springer-10.1007/s004310000587</subfield>
  </datafield>
  <datafield tag="100" ind1="1" ind2=" ">
   <subfield code="a">Lyon</subfield>
   <subfield code="D">Andrew</subfield>
   <subfield code="u">Simpson Memorial Maternity Pavilion, Lauriston Place, Edinburgh, EH3 9YW, Scotland e-mail: andy.lyon@ed.ac.uk Tel.: +44-131-5364213, Fax: +44-131-5364297, GB</subfield>
   <subfield code="4">aut</subfield>
  </datafield>
  <datafield tag="245" ind1="1" ind2="0">
   <subfield code="a">Chronic lung disease of prematurity. The role of intra-uterine infection</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Andrew Lyon]</subfield>
  </datafield>
  <datafield tag="520" ind1="3" ind2=" ">
   <subfield code="a">The clinical, radiological and pathological features of chronic lung disease have changed from those seen when the condition was first described. Most babies who now develop chronic lung disease have a birth weight below 1000 g and have only mild early respiratory disease, requiring minimal ventilation and low concentrations of inspired oxygen. The underlying pathophysiology of long-term lung damage appears to be a disturbance of the normal alveolar development which is continuing after birth, resulting in emphysematous like lungs with fewer and larger alveoli. Alveolarisation is affected by a number of insults including ventilation, oxygen, nutritional problems, steroids and both antenatal and post-natal infection. A final common pathway for many of these insults is persistence of an acute inflammatory response in the airways. There is good evidence that intra-uterine exposure to pro-inflammatory cytokines, as a consequence of ascending infection, induces both preterm labour and inflammation in the airways which triggers the lung injury sequence before birth. These cytokines have also been shown to have major effects on other organs in the body, in particular their association with brain damage and cerebral palsy. Treatment with antibiotics from birth has not been shown to affect the incidence or severity of chronic lung disease. Conclusion Intra-uterine infection is not only a common cause of preterm onset of labour but also a trigger to lung injury which significantly increases the risk of development of long-term respiratory disease in the newborn infant.</subfield>
  </datafield>
  <datafield tag="540" ind1=" " ind2=" ">
   <subfield code="a">Springer-Verlag Berlin Heidelberg, 2000</subfield>
  </datafield>
  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Key words Bronchopulmonary dysplasia</subfield>
   <subfield code="2">nationallicence</subfield>
  </datafield>
  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Chronic lung disease</subfield>
   <subfield code="2">nationallicence</subfield>
  </datafield>
  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Cytokines</subfield>
   <subfield code="2">nationallicence</subfield>
  </datafield>
  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Inflammation</subfield>
   <subfield code="2">nationallicence</subfield>
  </datafield>
  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Intra-uterine infection</subfield>
   <subfield code="2">nationallicence</subfield>
  </datafield>
  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">AbbreviationsIL interleukin</subfield>
   <subfield code="2">nationallicence</subfield>
  </datafield>
  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">TNFα tumour necrosis factor alpha</subfield>
   <subfield code="2">nationallicence</subfield>
  </datafield>
  <datafield tag="856" ind1="4" ind2="0">
   <subfield code="u">https://doi.org/10.1007/s004310000587</subfield>
   <subfield code="q">text/html</subfield>
   <subfield code="z">Onlinezugriff via DOI</subfield>
  </datafield>
  <datafield tag="908" ind1=" " ind2=" ">
   <subfield code="D">1</subfield>
   <subfield code="a">research-article</subfield>
   <subfield code="2">jats</subfield>
  </datafield>
  <datafield tag="950" ind1=" " ind2=" ">
   <subfield code="B">NATIONALLICENCE</subfield>
   <subfield code="P">856</subfield>
   <subfield code="E">40</subfield>
   <subfield code="u">https://doi.org/10.1007/s004310000587</subfield>
   <subfield code="q">text/html</subfield>
   <subfield code="z">Onlinezugriff via DOI</subfield>
  </datafield>
  <datafield tag="950" ind1=" " ind2=" ">
   <subfield code="B">NATIONALLICENCE</subfield>
   <subfield code="P">100</subfield>
   <subfield code="E">1-</subfield>
   <subfield code="a">Lyon</subfield>
   <subfield code="D">Andrew</subfield>
   <subfield code="u">Simpson Memorial Maternity Pavilion, Lauriston Place, Edinburgh, EH3 9YW, Scotland e-mail: andy.lyon@ed.ac.uk Tel.: +44-131-5364213, Fax: +44-131-5364297, GB</subfield>
   <subfield code="4">aut</subfield>
  </datafield>
  <datafield tag="900" ind1=" " ind2="7">
   <subfield code="a">Metadata rights reserved</subfield>
   <subfield code="b">Springer special CC-BY-NC licence</subfield>
   <subfield code="2">nationallicence</subfield>
  </datafield>
  <datafield tag="898" ind1=" " ind2=" ">
   <subfield code="a">BK010053</subfield>
   <subfield code="b">XK010053</subfield>
   <subfield code="c">XK010000</subfield>
  </datafield>
  <datafield tag="949" ind1=" " ind2=" ">
   <subfield code="B">NATIONALLICENCE</subfield>
   <subfield code="F">NATIONALLICENCE</subfield>
   <subfield code="b">NL-springer</subfield>
  </datafield>
 </record>
</collection>
