<?xml version="1.0" encoding="UTF-8"?>
<collection xmlns="http://www.loc.gov/MARC21/slim">
 <record>
  <leader>     caa a22        4500</leader>
  <controlfield tag="001">445884924</controlfield>
  <controlfield tag="003">CHVBK</controlfield>
  <controlfield tag="005">20180317145556.0</controlfield>
  <controlfield tag="007">cr unu---uuuuu</controlfield>
  <controlfield tag="008">170323e20110101xx      s     000 0 eng  </controlfield>
  <datafield tag="024" ind1="7" ind2="0">
   <subfield code="a">10.1007/s00011-010-0246-9</subfield>
   <subfield code="2">doi</subfield>
  </datafield>
  <datafield tag="035" ind1=" " ind2=" ">
   <subfield code="a">(NATIONALLICENCE)springer-10.1007/s00011-010-0246-9</subfield>
  </datafield>
  <datafield tag="100" ind1="1" ind2=" ">
   <subfield code="a">Rőszer</subfield>
   <subfield code="D">Tamás</subfield>
   <subfield code="u">Research Group of Apoptosis and Genomics, Hungarian Academy of Sciences, Debrecen, Hungary</subfield>
   <subfield code="4">aut</subfield>
  </datafield>
  <datafield tag="245" ind1="1" ind2="0">
   <subfield code="a">Inflammation as death or life signal in diabetic fracture healing</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Tamás Rőszer]</subfield>
  </datafield>
  <datafield tag="520" ind1="3" ind2=" ">
   <subfield code="a">Increased apoptosis of chondrocytes and osteoblasts and prolonged survival of osteoclasts lead to early destruction of callus tissue and impair bone remodeling in fracture healing of diabetic patients. Diabetes is accompanied by an increased inflammatory state, reactive oxgen species (ROS) generation and accumulation of advanced glycation end products (AGEs), a heterogenous group of toxic metabolites that can induce inflammation. Prolonged hyperglycemia and insulin resistance correlate with increased apoptosis rate and, accordingly, the proapoptotic role of several inflammatory mediators, ROS and AGEs has been also documented. In this review we summarize the most recent reports supporting the idea that inflammatory signaling increases chondrocyte and osteoblast death and prolongs osteoclast survival, resulting in impaired bone regeneration in diabetes. Antagonising inflammatory signal pathways and solution of inflammation may deserve greater attention in the management of diabetic fracture healing.</subfield>
  </datafield>
  <datafield tag="540" ind1=" " ind2=" ">
   <subfield code="a">Springer Basel AG, 2010</subfield>
  </datafield>
  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Diabetes mellitus</subfield>
   <subfield code="2">nationallicence</subfield>
  </datafield>
  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Apoptosis</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">Bone homeostasis</subfield>
   <subfield code="2">nationallicence</subfield>
  </datafield>
  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Regeneration</subfield>
   <subfield code="2">nationallicence</subfield>
  </datafield>
  <datafield tag="773" ind1="0" ind2=" ">
   <subfield code="t">Inflammation Research</subfield>
   <subfield code="d">SP Birkhäuser Verlag Basel</subfield>
   <subfield code="g">60/1(2011-01-01), 3-10</subfield>
   <subfield code="x">1023-3830</subfield>
   <subfield code="q">60:1&lt;3</subfield>
   <subfield code="1">2011</subfield>
   <subfield code="2">60</subfield>
   <subfield code="o">11</subfield>
  </datafield>
  <datafield tag="856" ind1="4" ind2="0">
   <subfield code="u">https://doi.org/10.1007/s00011-010-0246-9</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">review-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/s00011-010-0246-9</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">Rőszer</subfield>
   <subfield code="D">Tamás</subfield>
   <subfield code="u">Research Group of Apoptosis and Genomics, Hungarian Academy of Sciences, Debrecen, Hungary</subfield>
   <subfield code="4">aut</subfield>
  </datafield>
  <datafield tag="950" ind1=" " ind2=" ">
   <subfield code="B">NATIONALLICENCE</subfield>
   <subfield code="P">773</subfield>
   <subfield code="E">0-</subfield>
   <subfield code="t">Inflammation Research</subfield>
   <subfield code="d">SP Birkhäuser Verlag Basel</subfield>
   <subfield code="g">60/1(2011-01-01), 3-10</subfield>
   <subfield code="x">1023-3830</subfield>
   <subfield code="q">60:1&lt;3</subfield>
   <subfield code="1">2011</subfield>
   <subfield code="2">60</subfield>
   <subfield code="o">11</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>
