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21.
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
22.
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
23.
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
24.
25.
Computed tomography of abdominal fatty masses 总被引:2,自引:0,他引:2
26.
Relapsing polychondritis studied by computed tomography 总被引:1,自引:0,他引:1
Computed tomographic findings in a patient with relapsing polychondritis are described. Collapse of the cartilage of the nose and calcification in cartilages of the ears were clearly demonstrated. CT scanning was also helpful in evaluating the tracheobronchial tree for airway compromise, which could prove fatal in this condition. 相似文献
27.
本文研制了以四苯硼—唐松草新碱缔合物为电活性物质的变价态唐松草新碱—PVC膜电极。电极膜按电活性物质:PVC:DBP为1:8:8组成。该电极在pH 5.0~6.0,Ⅰ=0.05的NaCl—HCl溶液中Nernst响应范围为1×10-3~1×10-5mol/L。电极斜率为58.2 mV/logc。检测限为2.5×10-6mol/L。用直接电位法考察了TDH+,TDH2CF++共存时溶液pH和电极斜率S的关系。用S—pH关系,测定了25℃,Ⅰ=0.05时的Ka1值为(2.5±0.2)×10-4,用E—pH关系,测定了25℃,Ⅰ=0.05时的Ka2值为(8.1±0.9)×10-8。 相似文献
28.
29.
30.
Biosynthesis and secretion of factor VII, protein C, protein S, and the Protein C inhibitor from a human hepatoma cell line 总被引:7,自引:0,他引:7
Using specific radioimmunoassays, 8 day cultures of Hep G2 cells were shown to contain in their supernatants 16, 74, and 828 ng/mL and in their cell lysates, 8, 55, and 48 ng/2 X 10(8) cells of factor VII, protein C, and protein S, respectively. These proteins and the protein C inhibitor were functionally active, and each of these activities was neutralized by their respective polyclonal antibodies. Although vitamin K had a modest effect, warfarin decreased the activity of secreted factor VII, protein C, and protein S by 50% to 90%. Protein C and protein S antigens were reduced three- to fourfold by warfarin. The protein C inhibitor antigen and activity were unaffected by vitamin K or warfarin treatment. Intrinsic labeling and immunoprecipitation indicated that factor VII, protein S, and the protein C inhibitor were secreted as 52,000, 77,000, and 58,000 molecular weight (mol wt) proteins, respectively. Protein C was secreted as a single-chain protein of about 65,000 mol wt, indicating that all of the vitamin K- dependent proteins are translated and secreted as single-chain molecules. Each of the four proteins studied represented their plasma protein counterparts structurally, functionally, and immunochemically. Thus, all of the known soluble components of the protein C pathway are produced by liver parenchymal cells. 相似文献