Interest in herbal medication has increased because it appears to alleviate climacteric symptoms, while avoiding the risks of hormone replacement therapy (HRT), such as breast cancer or cardiovascu...
Traditionally, pathologists microscopically examine tissue sections to detect pathological lesions; the many slides that must be evaluated impose severe work burdens. Also, diagnostic accuracy varies by pathologist training and experience; better diagnostic tools are required. Given the rapid development of computer vision, automated deep learning is now used to classify microscopic images, including medical images. Here, we used a Inception-v3 deep learning model to detect mouse lung metastatic tumors via whole slide imaging (WSI); we cropped the images to 151 by 151 pixels. The images were divided into training (53.8%) and test (46.2%) sets (21,017 and 18,016 images, respectively). When images from lung tissue containing tumor tissues were evaluated, the model accuracy was 98.76%. When images from normal lung tissue were evaluated, the model accuracy ("no tumor") was 99.87%. Thus, the deep learning model distinguished metastatic lesions from normal lung tissue. Our approach will allow the rapid and accurate analysis of various tissues.
The expression of epithelial cell adhesion molecule (EpCAM) was investigated in early phase of hepatocarcinogenesis induced by diethylnitrosamine (DEN). Sixty ICR mice were divided into two groups and treated with saline (group 1) or DEN (group 2, 10 mg/kg of body weight, i.p. injection) at 14 days of age, and were sacrificed at 6 h and 1, 2, 3, 7, and 28 days after treatment of saline or DEN. At necropsy, half of the liver from salineor DEN-treated mice was processed for histopathological examination and immunohistochemical staining of EpCAM and apoptosis. And the remaining liver tissue was snapfrozen in liquid nitrogen for RNA extraction and analysis of EpCAM mRNA expression. Immunohistochemical examination showed that EpCAM expression was detected only in a small number of hepatocytes from saline-treated mice and its expression was detected in bile duct cells and round cells around portal area, as well as hepatocytes in the livers of DEN-treated mice. And multiple apoptotic cells were found in the liversof mice treated with DEN. EpCAM mRNA expression was significantly higher in DEN-treated mice at 1, 7, and 28 days compared to saline-treated ones at 6 h (P<0.01). Taken together, EpCAM expression and apoptosis were increased in liver by DEN treatment.
5716 As there may be increasing risk of heterocyclic amines in liver cancer, we investigated the enhancement carcinogenic potential of 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx), one of heterocyclic amines, in rats liver damage induced by thioacetamide (TAA). Rats (n=280) were divided into 14 groups. Animals of groups 1-7 received TAA (0.03%) for the first 12 weeks, and animals of groups 8-14 received drinking water without TAA. After withdrawal of TAA, all animals received MeIQx at doses from 0, 0.001, 0.01, 0.1, 1, 10 to 100 ppm (either groups 1-7 or groups 8-14, respectively) in pellet basal diet for 16 weeks. Animals of all groups were sacrificed at week 28. Numbers and area of glutathione S-transferase placental form (GST-P) positive foci, which are preneoplastic lesions of the liver, were increased significantly in all the groups received TAA→MeIQx compared to the groups treated with MeIQx alone (p
As exposure to heterocyclic amines might increase the risk of liver cancer, we investigated the carcinogenic potential of MeIQx under conditions of liver damage caused by TAA. Male, 6‐week‐old F344 rats ( n = 280) were divided into 14 groups; groups 1–7 received TAA (0.03% in drinking water) and groups 8–14 received water for the first 12 weeks. Thereafter, the animals received MeIQx at doses from 0, 0.001, 0.01, 0.1, 1, 10 to 100 p.p.m. (groups 1–7 and 8–14, respectively) in pellet basal diet for 16 weeks. All survivors were killed at week 28 for assessment of numbers and areas of GST‐P positive foci, considered to be pre‐neoplastic lesions of the liver. Values were increased significantly in all the groups receiving TAA→MeIQx compared to MeIQx alone ( P < 0.01). Numbers of GST‐P positive foci were significantly increased in groups 7 and 14 (treated with 100 p.p.m. MeIQx) as compared to 0 p.p.m.‐MeIQx (groups 1 and 8) ( P < 0.01), along with areas in group 14 compared to group 8 ( P < 0.01). However, with the maximum likelihood method, the data for numbers of GST‐P positive foci (groups 1–7 and groups 8–14) fitted the hockey stick regression model, representing no differences from groups 1–5 and from groups 8–13, despite a linear dose‐dependent increase of MeIQx‐DNA adducts from 0.1 to 100 p.p.m. We conclude that there is a no effect level for MeIQx hepatocarcinogenicity, even on a background of TAA‐induced liver damage. ( Cancer Sci 2006; 97)
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