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Studies have shown that nano-TiO2 can become enriched and toxic in multiple organs after entering the body through several methods, such as administration via the abdominal cavity or inhalation [7, 8].
Remarkably, mice that lack CHIP develop apoptosis in multiple organs after environmental challenge [52].
While apoptosis has been demonstrated in multiple organs after HS, it has not been previously demonstrated to occur within the heart following this insult.
Another factor contributing to perfusion impairment of multiple organs after asphyxia is endothelial cell swelling [ 18] which may cause shrinking of the vascular lumen by external pressure due to the interstitial edema [ 19].
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In summary, nano-TiO2 exhibited toxicity in multiple organs in mice after exposure through i.p. injection and gavage.
The phenotype of CTLA4 knock out mice, which develop massive T cell proliferation and autoimmune infiltration of multiple organs within weeks after birth, provides evidence of the critical role of CTLA4 in regulation of immune responses [6], [7].
This unexpected result warranted further inquiry, especially because exposure during such a narrow developmental window resulted in a specific set of teratogenic effects on multiple organs and tissues after only a short duration of atrazine exposure.
Six (67%) of nine septic shock patients who had developed complicated multiple organ failure after surgical operation survived after using PMX-20R.
In critically ill patients evaluation of StO2 demonstrated for example, that minimum StO2 predicted multiple organ failure after severe trauma patients [ 6] and after early goal-directed therapy of septic shock, a StO2 value below 78%% was associated with increased mortality at day 28 [ 7].
Preliminary tests revealed that isotope incorporations into multiple organs peaked ∼10 h after bolus ingestion.
OPN expression is upregulated in plasma and multiple organs (lungs and spleen) after sepsis in mice.
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