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@ARTICLE{Rhein:277477,
      author       = {S. Rhein and J. Inderhees and O. Herrmann and A. Othman and
                      K. Begemann and T. Fleming and P. P. Nawroth and K.
                      Klika$^*$ and R. Isa and I. R. König and G. Royl and M.
                      Schwaninger},
      title        = {{G}lyoxal in hyperglycaemic ischemic stroke - a cohort
                      study.},
      journal      = {Cardiovascular diabetology},
      volume       = {22},
      number       = {1},
      issn         = {1475-2840},
      address      = {London},
      publisher    = {BioMed Central},
      reportid     = {DKFZ-2023-01398},
      pages        = {173},
      year         = {2023},
      abstract     = {Hyperglycaemia is frequent in acute ischemic stroke and
                      denotes a bad prognosis, even in the absence of pre-existing
                      diabetes. However, in clinical trials treatment of elevated
                      glucose levels with insulin did not improve stroke outcome,
                      suggesting that collateral effects rather than
                      hyperglycaemia itself aggravate ischemic brain damage. As
                      reactive glucose metabolites, glyoxal and methylglyoxal are
                      candidates for mediating the deleterious effects of
                      hyperglycaemia in acute stroke.In 135 patients with acute
                      stroke, we used liquid chromatography coupled to tandem mass
                      spectrometry (LC-MS/MS) to measure glyoxal, methylglyoxal
                      and several of their glycated amino acid derivatives in
                      serum. Results were verified in a second cohort of 61 stroke
                      patients. The association of serum concentrations with
                      standard stroke outcome scales (NIHSS, mRS) was
                      tested.Glucose, glyoxal, methylglyoxal, and the
                      glyoxal-derived glycated amino acid
                      Nδ-(5-hydro-4-imidazolon-2-yl)ornithine (G-H1) were
                      positively correlated with a bad stroke outcome at 3 months
                      as measured by mRS90, at least in one of the two cohorts.
                      However, the glycated amino acids Nε-carboxyethyllysine
                      (CEL) and in one cohort pyrraline showed an inverse
                      correlation with stroke outcome probably reflecting lower
                      food intake in severe stroke. Patients with a poor outcome
                      had higher serum concentrations of glyoxal and
                      methylglyoxal.The glucose-derived α-dicarbonyl glyoxal and
                      glycated amino acids arising from a reaction with glyoxal
                      are associated with a poor outcome in ischemic stroke. Thus,
                      lowering α-dicarbonyls or counteracting their action could
                      be a therapeutic strategy for hyperglycaemic stroke.},
      keywords     = {Advanced glycation end-products (Other) / Glucose (Other) /
                      Ischemic brain damage (Other) / Undernutrition (Other)},
      cin          = {W160},
      ddc          = {610},
      cid          = {I:(DE-He78)W160-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37438755},
      doi          = {10.1186/s12933-023-01892-7},
      url          = {https://inrepo02.dkfz.de/record/277477},
}