Search PubMed⌕ Search

Biomedical subjects

R J Fry

Publications and source records attributed to R J Fry.

At least 73 records · Page 4Linked to original sources
PubMed1975

In vitro suppression of immunocompetent cells by lymphomas from aging mice.

We studied the effects of lymphomas in the spleens of aging (C57BL/6 X BALB/c)F1 (B6CF1) mice on the immunologic responsiveness of normal spleen cell cultures to sheep erythrocytes. The cultures were assayed for antibody-forming cells (AFC). Cultures of 20 times 10-6 normal spleen cells produced hundreds of AFC, whereas similar cultures of lymphomatous spleen cells produced less than ten AFC. Normal spleen cells were immunosuppressed in cultures with as few as 10-4 lymphomatous spleen cells. Our results demonstrated that lymphoma cells inhibited the response of normal spleen cells to antigenic stimulation in vitro. The age response for male mice gave a biphasic decline with a steeper second phase. This second decline of immune responsiveness started to appear as the incidence of lymphomas rose. This suggested that the immunosuppressive activity of lymphoma cells was causally related to the age-dependent decline of immune responsiveness in B6CF1 mice.

Aging↗
PubMed1975

Comparative enhancing effects of phenobarbital, amobarbital, diphenylhydantoin, and dichlorodiphenyltrichloroethane on 2-acetylaminofluorene-induced hepatic tumorigenesis in the rat.

Earlier studies showed that phenobarbital feeding enhanced hepatic tumorigenesis in rats previously fed 2-acetylaminofluorene for a brief period. As part of an investigation of the mechanism of this enhancement, the present study evaluated the relative enhancing abilities of amobarbital, diphenylhydantoin, and dichlorodiphenyltrichloroethane (DDT), agents that resemble phenobarbital to varying degrees in their effects on liver structure and metabolism. A comparison of hepatic tumor yields in rats fed 2-acetylaminofluorene, followed by the test substance (sequential treatment), showed that amobarbital and diphenylhydantoin had no enhancing activity, whereas the enhancing effect of DDT was similar to that of phenobarbital. These results show that the sequential treatment technique readily distinguishes among substances differing in enhancing ability and should prove useful in screening additional substances for this activity. The comparative biochemical effects of these substances in the liver can then be correlated with their relative enhancing abilities to provide information on the molecular events specifically associated with enhancement. Such correlations were initiated in this study by comparing the effects of the four test substances on liver weight and DNA synthesis. The results showed that the enhancers, phenobarbital and DDT, each stimulated liver DNA synthesis and increased liver weight, whereas the nonenhancers, amobarbital and diphenylhydantoin, had neither effect. Phenobarbital and DDT both increased the early tumor incidence rate and maintained an increment in tumor incidence over that in the other treatment groups throughout the experiment, although it is not clear whether this increment would persist indefinitely. In addition, although the spectrum of tumor types observed ranged from highly differentiated to poorly differentiated in all treatment groups, DDT and phenobarbital selectively increased the incidence of highly differentiated tumors throughout most of the experiment.

2-Acetylaminofluorene↗
PubMed1972

Analysis of survival and cause of death statistics for mice under single and duration-of-life gamma irradiation.

The late effects of protracted exposure to low levels of external radiation continue to be a matter of operational concern in long-range space flight. Studies have been carried out on young adult mice exposed to daily levels of 60Co gamma irradiation ranging from 0.3 to over 30 R day-1. The lowest level is comparable with the occupational maximum permissible dose for the atomic energy industry. There is little evidence of life shortening at that level, but as exposure increases, there is an exponential decline in life expectancy. The life-shortening coefficient is approximately 4 days/100 R accumulated or 4% R-1 day-1. When life-shortening is < or = 15%, all of the increased mortality can be attributed to radiation-induced increases in death rates from neoplastic diseases, including various forms of leukemia and pulmonary tumors. Age-specific death rates for mice dying of all other causes remain the same as the controls throughout life, at the lowest doses. A non-neoplastic disease component of excess mortality rate emerges at 6 R day-1 and above. The risk of death from all and specific causes following single exposures compared with protracted lifetime irradiation shows a clear effect of protraction. Leukemia death rates are reduced by a factor of 5 or more at all daily exposure levels below 20-30 R day-1. Risks for other causes of death are also reduced, but to a variable degree.

Animals↗