2003
DOI: 10.1016/s0022-4804(03)00199-9
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Cold ischemic injury, aortic allograft vasculopathy, and pro-inflammatory cytokine expression

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Cited by 11 publications
(10 citation statements)
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“…Since cold ischemia time is a risk factor for late transplant loss, this study was primarily undertaken to show that cold preservation alone can give rise to profound intimal hyperplasia, even in the absence of an allo‐immune response. Hence, our study emphasizes the pivotal role of cold preservation damage on vascular remodeling and is in line with previous studies on the influence of cold preservation on vascular function and remodeling [31,32]. Our studies are also in line with a recent report by Nakao et al.…”
Section: Discussionsupporting
confidence: 93%
“…Since cold ischemia time is a risk factor for late transplant loss, this study was primarily undertaken to show that cold preservation alone can give rise to profound intimal hyperplasia, even in the absence of an allo‐immune response. Hence, our study emphasizes the pivotal role of cold preservation damage on vascular remodeling and is in line with previous studies on the influence of cold preservation on vascular function and remodeling [31,32]. Our studies are also in line with a recent report by Nakao et al.…”
Section: Discussionsupporting
confidence: 93%
“…Low temperature could also increase the proportion (IL-12/IL-10 and TNF-a/IL-10) of proinflammatory cytokines that leading to inflammation. On the other hand, cold stimulation could induce the activity of SLE by inducing cell apoptosis [15][16][17][18][19][20]. Consistent with this, we found that there were more active SLE patients in winter and spring; this may be due to increasing opportunities that the SLE patients exposure to cold stimulation so that proinflammatory cytokines accumulated in the body and increased clinical symptoms.…”
Section: Discussionsupporting
confidence: 83%
“…[37][38][39] On the other hand, cold stimulation could induce the injury of blood vessels that may aggravate the renal vasculopathy induced by SLE. 40 In contrast to adaptive compensatory increases in RBC production observed in healthy people after exposure to systemic hypoxia at high altitudes, 41 we found that the RBC counts and hemoglobin level in patients at high altitudes were lower than those at moderate and/or low altitudes, although there was no significant association between altitudes and hematologic changes as shown in Table 1. In contrast, we observed the lowest level of platelet counts in patients at high altitudes, which were consistent with changes of platelet counts in the normal population affected by high altitudes.…”
Section: Discussioncontrasting
confidence: 57%