On March 31, 2019, Shang, Jijun; Corriveau, Jeanne; Champoux-Jenane, Alexandre; Gagnon, Julie; Moss, Emmanuel; Dumas, Pierre; Gaudreau, Eric; Chevrier, Jonathan; Chalifour, Lorraine E. published an article.Electric Literature of 3319-31-1 The title of the article was Recovery from a myocardial infarction is impaired in male C57bl/6N mice acutely exposed to the bisphenols and phthalates that escape from medical devices used in cardiac surgery. And the article contained the following:
Bisphenols and phthalates leach from medical devices, and this exposure is likely to increase in postcardiac surgery patients. Previous studies suggest that such chem. exposure may impact recovery and wound healing, yet the direct effects of bisphenols and phthalates are unknown in this context. To study the direct effect of clin. based chem. exposures, we measured the metabolites representative of 6 bisphenols and 10 phthalates in men before and after cardiac surgery and then replicated this exposure in a mouse model of cardiac surgery and assessed survival, cardiac function and inflammation. Bisphenol A (BPA), di-Et hexyl phthalate (DEHP), butylbenzyl phthalate, di-isodecyl phthalate, and di-Bu phthalate metabolites were increased after surgery. DEHP exposure predominated, was pos. correlated with duration on the cardiopulmonary bypass machine and exceeded its tolerable daily intake limit by 37-fold. In vivo, C57bl/6N male mice treated with BPA+phthalates during recovery from surgery-induced myocardial infarction had reduced survival, greater cardiac dilation, reduced cardiac function and increased infiltration of neutrophils, monocytes and macrophages suggesting impaired recovery. Of interest, genetic ablation or estrogen receptor beta (ERβ) antagonism did not improve recovery and replacement of DEHP with tri-octyl trimellitate or removal of BPA from the mixture did not ameliorate these effects. To examine the direct effects on inflammation, treatment of human THP-1 macrophages with BPA and phthalates induced a dysfunctional proinflammatory macrophage phenotype with increased expression of M1-type macrophage polarization markers and MMP9 secretion, yet reduced phagocytic activity. These results suggest that chems. escape from medical devices and may impair patient recovery. The experimental process involved the reaction of Tris(2-ethylhexyl) benzene-1,2,4-tricarboxylate(cas: 3319-31-1).Electric Literature of 3319-31-1
The Article related to myocardial infarction heart surgery medical device bisphenol phthalate inflammation, bisphenol a, estrogen receptor, macrophage, medical devices, myocardial infarction, phthalates and other aspects.Electric Literature of 3319-31-1
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