Digestive System 1

Greaves, Peter

doi:10.1016/b978-044450514-9/50007-3

Cited by 4 publications

(4 citation statements)

References 406 publications

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“…The lesions in the adrenal cortex (rats - hypertrophy and fatty degeneration in the cytoplasm of cells in the zona fasciculate) and in the non glandular and/or glandular stomach mucosa (rats and mice - erosions and/or ulceration and inflammation) were considered to be stress related (Greaves, 2000a; Greaves, 2000b). The presence of abnormal residual body formation in the high dose mouse testes was suggestive of a primary effect on the sustentacular Sertoli cells (Melnick et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Characterization of liver toxicity in F344/N rats and B6C3F1 mice after exposure to a flame retardant containing lower molecular weight polybrominated diphenyl ethers

Dunnick

Nyska

2009

Experimental and Toxicologic Pathology

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Lower molecular weight polybrominated diphenylethers (PBDEs), components of flame retardants, are found in the environment and in human and animal tissues. Toxicity studies were conducted in F344/N rats and B6C3F1 mice by administering a flame retardant containing these lower molecular weight PBDEs (BDE-47, BDE-99, BDE-100, and BDE153) by oral gavage 5 days/week for 13 weeks at doses of 0.01, 5, 50, 100 or 500 mg/kg/day. Liver was the primary target organ in rats and mice. Treatment-related increases in liver weights, liver cytochrome P450 (1A1, 1A2, 2B) and UDPGT (rats only) levels, and liver lesions were seen in both rats and mice. Hepatocyte hypertrophy and vacuolization increased in incidence and severity with treatment, and occurred at levels of 50 mg/kg and above in rats, and at 100 mg/kg and above in mice. Liver Cyp 1A1, 1A2, and 2B levels were increased at exposure levels of 50 mg/kg and above in rats and mice. In addition, treatment-related thyroid lesions occurred particularly in rats. The most sensitive parameter for PBDE toxicity was the increase in liver weights which occurred at 5 mg/kg above in rats and 50 mg/kg and above in mice. These results suggest that liver may be a target organ for carcinogenesis processes after long-term administration of PBDEs. A chronic PBDE study is currently being conducted by the National Toxicology Program.

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Section: Discussionmentioning

confidence: 99%

Characterization of liver toxicity in F344/N rats and B6C3F1 mice after exposure to a flame retardant containing lower molecular weight polybrominated diphenyl ethers

Dunnick

Nyska

2009

Experimental and Toxicologic Pathology

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“…They are most commonly caused by antisecretory drugs (3,7,12,27,31,34) and are more common in rats than mice. This higher incidence in rats is probably because rats are more endowed with ECL cells, the cell type constituting the tumors (9). The mechanism of induction of carcinoids has been referred to as the "gastrin hypothesis" (3, 5, 7, 10-12, 17, 35).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, neuroendocrine tumors rarely occur in control mice in standard 1.5-year CD-1 mouse oncogenicity studies. However, the chance of detecting this type of tumor is greater in extended 2-year studies (3,9). Background data on the spontaneous incidence of gastric neuroendocrine tumors in 2-year studies are scarce, and a single case, with metastasis to regional lymph nodes, was found in B6C3F1 mice (18,22).…”

Section: Discussionmentioning

confidence: 99%

Gastric Neuroendocrine Tumors in a 2-Year Oncogenicity Study With CD-1 Mice

et al. 2002

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Descriptions of two rare gastric neuroendocrin e tumors (carcinoids) of enterochromaf n (ECL) cells in CD-1 mice (2/50) from a 104-week oncogenicity study of a serotonergic/dopaminergi c compoun d are presented. These tumors were detected at necropsy and con rmed by histopathology in hematoxyli n and eosin-and Chromogranin A-stained slides. ECL cell counts of the glandular stomachs were determined by quantitative image analysis and did not reveal any hyperplasti c changes as possible predisposing lesions for carcinoid formation. To investigate the possibility of druginduced hypergastrinemi a as the cause of tumor formation of ECL cells, gastrin blood levels were measured after treating mice for 7 days with the test substance. In this study, Omeprazole, the positive control, raised gastrin levels, while the test material did not. It was concluded that these two tumors were an example of "late-life"-occurring, spontaneous neuroendocrin e tumors in the stomachs of aged CD-1 mice.

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“…Once (proto-)planets have been formed, they may significantly alter the surface density profile of the disk and thus cause signatures in the disk that are much easier to find than the planets themselves. The appearance and type of these signatures depend on the mass and orbit of the planet, but even more on the evolutionary stage of the circumstellar disk: While the spatial structure of optically thick, young circumstellar disks around Herbig AejBe and T Tauri stars is dominated by gas dynamics, the much lower optical depth and gas-to-dust mass ratios in debris disks (Zuckermann, Forveille, & Kastner 1995;Dent et al 1995;Artymowicz 1997;Liseau & Artymowicz 1998;Greaves, Coulson, & Holland 2000) let the stellar radiation via Poynting-Robertson effect and stellar wind drag, in addition to gravitation, be responsible for the resulting disk density distribution. Left: Azimuthally averaged disk surface density for planets with masses of 0.01 -1 MJupiter.…”

Section: Mapping Planet -Disk Interactionsmentioning

confidence: 99%