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These empirical models provided a means of quantifying the effects of CP on YL.
They investigated the effects of CP on the length of hospital stay, complications, hospital cost, and functional outcomes.
However, no study has been conducted to demonstrate the effects of CP on vascular injury-related brain disease.
The damaging effects of CP on ovarian follicles have been previously reported by numerous investigators [ 4, 5, 28].
We examined the effects of CP on chronic BCCAo-induced MBP breakdown in the medial septum, corpus callosum, fimbria, fornix of the white matter, and hippocampus.
Therefore, to examine the effects of CP on BCCAo-induced inflammation, we used western blotting to measure hippocampal levels of COX-2, IL-1β, and IL-6.
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Based on recent results, cultures of primary rat hepatocytes and pneumocytes have been selected as key cellular models in the investigation of possible adverse effects of CPs on the DNA level and thus their genotoxicity [ 28– 30].
In order to illustrate the behavioral regulation of the rare minnow in CP stress, the current study was therefore performed to assess the effects of CPs on the aquatic environment by examining the behavioral effects of arprocarb, carbofuran, and oxamyl with an online monitoring system and Self-Organizing Map analysis.
Lastly, we examined an in vivo effect of CP on innate immune response in arthritis using K/BxN serum transfer arthritis model and found that CP treatment significantly inhibited inflammation and joint swelling.
Data presented in Table 1 and Fig. 4 showed the genotoxic effect of CP on hepatocytes and the protective role of ABG.
To our knowledge, there has not yet been any reported evaluation by ultrasonography of the effect of CP on distal femoral cartilage.
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