Background: Although epidemiological studies indicate that ethanol consumption and the risk of breast cancer are positively associated in women, experimental animal models have not yet been developed that provide evidence to support this relationship. To clarify alcohol‐related liver injury, it is important to reproduce, in laboratory small animals, the liver fibrosis observed in human alcoholics. However, in mice the induction of fibrosis has failed. The present study describes the first experimental models to produce mammary tumors in female ICR mice and liver fibrosis in male ICR mice treated long‐term with ethanol.Methods: The study consisted of two parts. To induce mammary tumors, female ICR mice were given 10% to 15% ethanol solution as the sole drinking fluid for 25 months, with solid diet supplied ad libitum. To induce liver fibrosis, male ICR mice were given 10% to 15% ethanol solution as the sole drinking fluid for 10 to 15 months. Control female and male mice were given tap water.Results: In 9 (45%) of 20 ethanol‐treated female mice, mammary tumors occurred at 8 to 24 months after ethanol intake began, whereas spontaneous mammary tumor was not found in the 20 control female mice. The tumors were composed histopathologically of either papillary adenocarcinoma or medullary adenocarcinoma of glandular epithelial origin. In the ethanol‐treated male mice, early hepatic fibrosis at the centrilobular and pericellular areas and central‐central bridging were observed at the 10th month, and marked fibrosis at the centrilobular, pericellular, and periportal areas and bridging between the neighboring vascular tissues were observed at the 15th month, which suggested that the initial fibrosis arose from the centrilobular area. No abnormalities other than mild fatty infiltration were found in livers of the control male mice.Conclusions: These murine models may be useful to study the role of ethanol in mammary tumorigenesis and the pathogenetic mechanisms of ethanol liver injury.
The plankton test (generally, diatom test) is one of the methods available to diagnose the cause of death of submerged bodies. The solubilization method using tissue solubilizer Soluene-350 was used in this study to detect not only diatoms but also green algae, based on the fact that the solubilizer does not digest the cell walls of green algae which are made from cellulose. Detection of green algae from organs of submerged cadavers is very informative to determine drowning in fresh water, and also in cases where only few diatoms are detected in the organs.
Using primers designed by Lee and Chang, 200 base-pair (bp) fragment of ABO locus was amplified by PCR, which spans the site of the single nucleotide deletion associated with O allele. O allele could be identified by Kpn I digestion of the PCR product as reported. A and B alleles were also distinguishable by Mae II digestion of the product. Thus restriction digestion by Kpn I and Mae II could genotype ABO blood group following the single amplification. The nucleotide substitution in the 200-bp product between A and B alleles was also found in O allele, resulting in 2 different suballeles OA and OG. The single-strand conformational polymorphism of the PCR product was also investigated for ABO genotyping following the single amplification.
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