Abnormal esophageal acid exposure was demonstrated in 62%, with pharyngeal reflux documented in 30%.
The importance of entire life cycle study to better evaluate cladoceran responses to chronic dietary metal exposure was demonstrated.
Moreover, the apoptotic effect of imatinib (10 μM, 50 μM) after 24 h of exposure was demonstrated as evaluated by translocation of phosphatidylserine to external membrane leaflet and by increased activity of caspase-3.
Less than proportional increase in exposure was demonstrated over the 3 9 mg/kg dose range, though post hoc analysis showed dose proportionality was more feasible over the 3 6 mg/kg range.
After 24 h, significantly less phosphatidylserine exposure was demonstrated in the HCO group, whereas no difference in DNA fragmentation or caspase-3 activity was found.
GC exposure was demonstrated to impair various pathways in the β-cell in vitro.
A clear relationship between hepatomegaly at 1 year after exposure and a positive tumorigenic outcome at 18 months or 2 years after exposure was demonstrated.
The chronology of exposure was demonstrated: the preoperative urine and serum levels of the DEHP metabolites were often below the detection limit.
The cumulative effect of AER on exposure was demonstrated by statistical differences in CCR between participants who lived in homes with ventilation rates < 0.5/hr and > 1/hr.
In both NALM-6 and KG-1a cells, a dose-dependent reduction of S-phase proliferating cells after PFT-μ exposure was demonstrated.
