39 research outputs found

    Values of maximal relaxation (R<sub>max</sub>,%) and pD<sub>2</sub> to acetylcholine (ACh), to sodium nitroprusside (SNP) and contraction forces induced by phenylephrine (10<sup>-6</sup>M) in aortic rings in control, ischemic storage, ischemic storage and in vitro reperfusion, ischemic storage and in vivo 2h reperfusion, ischemic storage and in vivo 24h reperfusion, ischemic storage and in vivo 7d reperfusion group.

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    <p>Values represent mean ± SEM</p><p><sup><i>a</i></sup> P<.05 versus control</p><p><sup><i>b</i></sup> P<.05 versus ischemic storage</p><p><sup><i>c</i></sup> P<.05 versus ischemic storage + in vitro reperfusion</p><p><sup><i>d</i></sup> P<.05 versus ischemic storage + in vivo 2h reperfusion</p><p><sup><i>e</i></sup> P<.05 versus ischemic storage + in vivo 24h reperfusion</p><p><sup><i>f</i></sup> P<.05 versus ischemic storage + in vivo 7d reperfusion.</p><p>Values of maximal relaxation (R<sub>max</sub>,%) and pD<sub>2</sub> to acetylcholine (ACh), to sodium nitroprusside (SNP) and contraction forces induced by phenylephrine (10<sup>-6</sup>M) in aortic rings in control, ischemic storage, ischemic storage and in vitro reperfusion, ischemic storage and in vivo 2h reperfusion, ischemic storage and in vivo 24h reperfusion, ischemic storage and in vivo 7d reperfusion group.</p

    Gene expressions of (A) Bax, (B) Bcl-2, (C) caspase-3 and (D) endothelial nitric oxide synthase (eNOS) in aortic rings.

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    <p>Controls were given the arbitrary value of 1. Values represent median ± quartiles; *P<.05 versus control; #P<.05 versus ischemic storage; ‡P<.05 versus ischemic storage and in vitro reperfusion; †P<.05 versus ischemic storage and in vivo 2h reperfusion.</p

    DNA strand breaks and CD-31 positive cells in aortic rings.

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    <p>(A) endothelium-covered area (in percentage of the lumen area) (B) scoring of TUNEL staining (in percentage of total cell number) (Magnification x200, bar = 50μm) Values represent mean ± SEM; *P<.05 versus control; #P<.05 versus ischemic storage; §P<.05 versus ischemic storage and in vitro reperfusion; $P<.05 versus ischemic storage and in vivo 2h reperfusion.</p

    AGE accumulation in MCF-7 and TamR cells.

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    <p>MCF-7-Md and TamR-Md cells were grown under standard conditions and harvested in the logarithmic phase. Cells were fractionated by a detergent based protocol and AGEs detected by Western blotting. Based on protein determination and Coomassie staining (A), equal amounts of protein were loaded for both cell lines and the AGEs MG-AGE (B) and CML (C) detected by Western analysis. Differences in the pattern of AGE-modified proteins are indicated by arrows.</p

    AGE accumulation under exogenous aldehyde stress.

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    <p>A: AGE accumulation (CML (left) and MG-AGE (right)) in MCF-7-Md (lower panel) and TamR-Md cells (upper panel) after cultivation for three days with different concentrations of methylglyoxal and glyoxal as shown by Western blotting. Strongly enhanced AGE accumulation became visible when cell number was significantly reduced due to toxic effects, as represented by the decreasing β-actin signal. Glyoxal resulted in accumulation of CML whereas methylglyoxal treatment caused MG-AGE modification. Cells were treated as described for the determination of vitality/proliferation. Proteins were extracted per well and not corrected for protein amount. Therefore, the blots represent adherent cells only. B) AGE accumulation shown by immunofluorescence. Composite images of dual exposures are shown. MCF-7-Md cells were stained for CML and MG-AGE (red) by specific antibodies as indicated and nuclear staining was achieved with DAPI (blue) of cells treated for 24 h with 1 mM methylglyoxal or glyoxal.</p

    Kinase phosphorylation in MCF-7-Md and TamR-Md cells in response to glyoxal and methylglyoxal.

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    <p>Confluent and serum starved cells were incubated with different concentrations of dicarbonyls for 10 minutes before proteins were extracted and subjected to Western blot analysis. Experiments were repeated three times in duplicate. A representative Western blot and the quantification of the signals of all experiments are shown. Band intensity was expressed relative to the β-actin signal and control treatments were set to 1 for each cell-line.</p
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