Mammary gland dysplasia and postpartum hypogalactia often occur in humans and in the livestock breeding industry. However, their underlying mechanisms are not clear yet. Mifepristone, which has a high affinity for progesterone (P 4 ) and glucocorticoid receptors, was exploited here to induce the disorders of mammary gland development and lactation. Four strategies were devised for treating pregnant mice with mifepristone. In the first strategy, mice were administered 1.20 mg mifepristone/kg body weight (BW) on pregnancy day 4 (Pd4). In the second strategy, mifepristone was administered to mice twice, with 1.20 mg/kg BW on Pd4 and 0.40 mg/kg BW on Pd8. In the third strategy, mice were treated with a single dose of 0.40 mg mifepristone/kg BW on Pd8. In the fourth strategy, mice were administered 0.40 mg mifepristone/kg BW on Pd8 and 0.20 mg mifepristone/kg BW on Pd12. The results suggested that mifepristone administration at the dose of 1.20 mg/kg BW on Pd4 caused significant reduction in milk production on lactation day 1 (Ld1), Ld2, and Ld3, as assessed using a weighsuckle-weigh assay. Mammary β-casein expression, milk yields, litter growth rates, gland structure, and serum concentrations of 17-β estrogen (E 2 ), P 4 , prolactin (PRL), growth hormone (GH), corticosterone (CORT) and oxytocin (OT) as well as the receptors of these hormones were determined during pregnancy or lactation after performing the first (Pd4) strategy. The results demonstrated that mifepristone administration during early pregnancy decreased β-casein expression, milk yields and litter growth rates, induced fewer alveoli, enlarged alveolar lumina, and altered the levels of E 2 , P 4 , PRL, GH, CORT, and OT as well as the mRNA expression of these hormonal receptors during pregnancy or early lactation. The present study on pregnant mice treated with mifepristone offers an innovative murine model to study the mechanism underlying mammary gland dysplasia and postpartum hypogalactia.

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The objective of this study was to provide the characteristics of hepatic computed tomography images and optimize their transition delay with a bolus-tracking technique for triple-phase hepatic computed tomography in cats. Dynamic triple-phase computed tomography was performed in nine healthy cats. The upper third of the liver was dynamically scanned every 0.5 s for 40 s. The time density curves of the aorta and hepatic parenchyma mean enhancement were analyzed. Triple-phase hepatic computed tomography was performed three times with a bolus trigger of 200 Hounsfield units of aortic enhancement. The transition delays of the arterial, portal, and hepatic parenchymal phases were respectively 0, 5 and 60 s in the first scan; 2, 7 and 62 s in the second scan; and 4, 9 and 64 s in the third scan. All computed tomography images were evaluated by a certificated radiologist. The arterial vessels and their main branches were well enhanced at a 2 s transition delay. The contrast of the portal vein to the liver parenchyma was most obvious at a 7 s transition delay. The mean enhancement of the hepatic parenchyma peaked at a 62 s transition delay, whereas the degree of enhancement of the hepatic vasculature decreased. In this study, the recommended transition delays for the arterial, portal, and hepatic parenchymal phases were 2 s, 7 s and 62 s, respectively, after triggering at 200 Hounsfield units of aortic enhancement. This information may be helpful in diagnosing feline liver diseases and provides a key reference for the clinical implementation of CT.