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Resistance of Copenhagen rats to chemical induction of glutathione S- transferase 7-7-positive liver foci 总被引:2,自引:0,他引:2
Copenhagen (Cop) rats are completely resistant to the chemical induction of
mammary adenocarcinomas, but their susceptibility to hepatocarcinogenesis
is virtually unknown. Rat liver is a well- characterized and easily
manipulated tissue in which to study carcinogenesis. Therefore, if Cop rats
are resistant to hepatocarcinogenesis, studies into resistance mechanisms
may be feasible. Male Cop and F344 rats, 7-8 weeks old, were initiated
using either N-nitrosodiethylamine (DEN) (200 mg/kg, i.p.) or a two-thirds
partial hepatectomy (PH) followed by N-methyl-N-nitrosourea (MNU) (60
mg/kg, i.p.). The rats were then promoted using a modified resistant
hepatocyte (RH) protocol (a combination of four doses of 2-
acetylaminofluorene (2-AAF) and a single dose of CCl4 that provides a
selective mitotic stimulus for initiated cells). Six weeks after initiation
the rats were killed and liver sections were stained for glutathione
S-transferase 7-7 (GST 7-7), a marker for putative preneoplastic
hepatocytes. Cop rats were found to be highly resistant, having a
approximately 9- and approximately 27-fold smaller percentage of liver area
occupied by GST 7-7-positive foci than susceptible F344 rats following
initiation by DEN and MNU respectively. Furthermore, gross liver nodules
did not form in any of the Cop rats, whereas all F344 rat livers contained
nodules. Hepatic necrosis caused by DEN during initiation, and CCl4 during
promotion is necessary to stimulate compensatory hepatocyte division. We
demonstrated that these agents do indeed increase serum transaminase levels
and produce histologic evidence of necrosis in Cop rats. In order for liver
foci to grow rapidly in the RH protocol, the surrounding normal hepatocytes
must be mito-inhibited by 2-AAF. We found that the degree of
mito-inhibition of normal hepatocytes by 2-AAF is the same in Cop and F344
rats. These results show that the Cop rat is highly resistant to the
chemical induction of putative preneoplastic liver foci and nodules.
相似文献
25.
DS Wilensky G Ginsberg M Altman TH Tulchinsky F Ben Yishay J Auerbach 《Archives of disease in childhood》1996,75(2):145-148
OBJECTIVE: To examine the characteristics of infants suffering from failure to thrive in a community based cohort in Israel and to ascertain the effect of failure to thrive on their cognitive development. METHODS: By review of records maintained at maternal and child health clinics in Jerusalem and the two of Beit Shemesh, epidemiological data were obtained at age 15 months on a cohort of all babies born in 1991. For each case of failure to thrive, a matched control was selected from the same maternal and child health clinic. At age 20 months, cognitive development was measured, and at 25 months a home visit was carried out to assess maternal psychiatric status by questionnaire, and the HOME assessment was performed to assess the home environment. RESULTS: 3.9% of infants were found to have fallen below the third centile in weight for at least three months during the first year of life. Infants with failure to thrive did not differ from the general population in terms of obstetric or neonatal complications, birth order, or parents' ethnic origin, age, or years of education. The infants with failure to thrive did have lower birthweights and marginally smaller head circumferences at birth. Developmental assessment at 20 months of age showed a DQ of 99.7 v 107.2 in the matched controls, with 11.5% having a DQ below 80, as opposed to only 4.6% of the controls. No differences were found in maternal psychiatric problems as measured by a self report questionnaire. There were, however, significant differences in subscales of the HOME scale. CONCLUSIONS: (1) Infants who suffered from failure to thrive had some physiological predispositions that put them at risk; (2) failure to thrive may be an early marker of families providing suboptimal developmental stimulation. 相似文献
26.
Wound bed preparation: a systematic approach to wound management 总被引:6,自引:0,他引:6
Gregory S.Schultz PhD ; R. GarySibbald MD ; VincentFalanga MD ; Elizabeth A.Ayello PhD ; CarolineDowsett ; KeithHarding MB ChB ; MarcoRomanelli MD PhD ; Michael C.Stacey DS ; LucTeot MD PhD ; WolfgangVanscheidt MD 《Wound repair and regeneration》2003,11(S1):S1-S28
The healing process in acute wounds has been extensively studied and the knowledge derived from these studies has often been extrapolated to the care of chronic wounds, on the assumption that nonhealing chronic wounds were simply aberrations of the normal tissue repair process. However, this approach is less than satisfactory, as the chronic wound healing process differs in many important respects from that seen in acute wounds. In chronic wounds, the orderly sequence of events seen in acute wounds becomes disrupted or "stuck" at one or more of the different stages of wound healing. For the normal repair process to resume, the barrier to healing must be identified and removed through application of the correct techniques. It is important, therefore, to understand the molecular events that are involved in the wound healing process in order to select the most appropriate intervention. Wound bed preparation is the management of a wound in order to accelerate endogenous healing or to facilitate the effectiveness of other therapeutic measures. Experts in wound management consider that wound bed preparation is an important concept with significant potential as an educational tool in wound management.
This article was developed after a meeting of wound healing experts in June 2002 and is intended to provide an overview of the current status, role, and key elements of wound bed preparation. Readers will be able to examine the following issues;
• the current status of wound bed preparation;
• an analysis of the acute and chronic wound environments;
• how wound healing can take place in these environments;
• the role of wound bed preparation in the clinic;
• the clinical and cellular components of the wound bed preparation concept;
• a detailed analysis of the components of wound bed preparation.
(WOUND REP REG 2003;11:1–28) 相似文献
This article was developed after a meeting of wound healing experts in June 2002 and is intended to provide an overview of the current status, role, and key elements of wound bed preparation. Readers will be able to examine the following issues;
• the current status of wound bed preparation;
• an analysis of the acute and chronic wound environments;
• how wound healing can take place in these environments;
• the role of wound bed preparation in the clinic;
• the clinical and cellular components of the wound bed preparation concept;
• a detailed analysis of the components of wound bed preparation.
(WOUND REP REG 2003;11:1–28) 相似文献
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28.
S Parangi M O''Reilly G Christofori L Holmgren J Grosfeld J Folkman D Hanahan 《Proceedings of the National Academy of Sciences of the United States of America》1996,93(5):2002-2007
Angiogenesis is activated during multistage tumorigenesis prior to the emergence of solid tumors. Using a transgenic mouse model, we have tested the proposition that treatment with angiogenesis inhibitors can inhibit the progression of tumorigenesis after the switch to the angiogenic phenotype. In this model, islet cell carcinomas develop from multifocal, hyperproliferative nodules that show the histological hallmarks of human carcinoma in situ. Mice were treated with a combination of the angiogenesis inhibitor AGM-1470 (TNP-470), the antibiotic minocycline, and interferon alpha/beta. The treatment regimen markedly attenuated tumor growth but did not prevent tumor formation; tumor volume was reduced to 11% and capillary density to 40% of controls. The proliferation index of tumor cells in treated and control mice was similar, whereas the apoptotic index was doubled in treated tumors. This study shows that de novo tumor progression can be restricted solely by antiangiogenic therapy. The results suggest that angiogenesis inhibitors represent a valid component of anticancer strategies aimed at progression from discrete stages of tumorigenesis and demonstrate that transgenic mouse models can be used to evaluate efficacy of candidate antiangiogenic agents. 相似文献
29.
S O Daunt K E Kotowski A P O''Reilly A T Richardson 《Sexually transmitted infections》1982,58(6):405-407
In a case of acute Reiter's syndrome with severe vulvitis the diagnosis was based on the presence of a vaginal discharge and dysuria, arthritis, conjunctivitis, buccal ulceration, keratodermia blenorrhagica, and HLA B27 tissue-typing antigen. The vulval lesions were similar in appearance to those of circinate vulvitis. The acute histological change were confined to shallow ulceration with an inflammatory infiltration of the subjacent dermis. Coincidential lichen sclerosus et atrophicus was present, which could have been masked by the acute lesions. 相似文献
30.
Computed tomography of abdominal fatty masses 总被引:2,自引:0,他引:2