Sentence examples for models for arsenic from inspiring English sources
The column experimental data were fitted well to the Adam Bohrat, Thomas and Yoon Nelson models for arsenic feed concentrations from 15 to 30 ppb at the flow rate of 7mL/minn.
The parametric comparison between human and rat hepatocyte TK models for arsenic, presented in Table 2, provides insight into factors that affect arsenic metabolism in hepatocytes.
Lysine and arginine methyltransferases are good models for arsenic methyltransferases, as they carry out three very similar methyl transfers without oxidation of the nitrogen.
Because animal models for arsenic carcinogenesis are currently absent for the prostate, this in vitro system has been used to help define the molecular events in arsenic-induced prostatic carcinogenesis.
However, mice do not develop arsenic-related bladder cancer, so the mouse may not be the best model for arsenic carcinogenesis in humans.
Although epidemiologic evidence shows an association between inorganic arsenic in drinking water and increased risk of skin, lung, and bladder cancers, no animal model for arsenic carcinogenesis has been successful.
They best fit a nonlinear or threshold carcinogenic risk model for arsenic with an inflection point at 150 μg/L (Taiwan) with the presence of at least one additional confounding risk factor.
Failure to find an animal model for arsenic carcinogenesis might be because arsenite is not a carcinogen per se but acts as an enhancing agent (cocarcinogen) with a genotoxic partner.
In contrast, the only currently existing cellular level TK model for arsenic, from Easterling et al. [ 34], was parameterized using the same optimization technique and data, but the model was not able to adequately capture these modes (shown in Figure 4, Row 2).
We chose to adjust all models for cumulative arsenic exposure instead of average arsenic exposure or urinary arsenic concentrations.
Recent animal models for inorganic arsenic carcinogenesis suggest that the carcinogenicity of arsenic involves several mechanisms and co-exposure to other carcinogens (Burns et al. 2004; Cohen et al. 2007; Rossman et al. 2004; Waalkes et al. 2007; Wanibuchi et al. 2004).
