R.H. Mole
Medical Research Council
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Featured researches published by R.H. Mole.
International Journal of Radiation Biology | 1962
J.A.H. Brown; M.J. Corp; R.H. Mole
Summary1. Changing the exposure time from 15 min to less than 1 min and the dose-rate from 54 to 1100 rads/min did not reduce the LD50/30 by more than a few per cent. Changes in the uniformity of tissue dose, as by changing the direction of the x-ray beam, were quantitatively much more important.2. The effect of increasing exposure time from 6 to 36 hours with continuous irradiation was compared with other exposures spread over similar periods of time but divided into 2, 4 or 18 equal fractions, each at a relatively high dose-rate. Neither with continuous nor with fractionated exposures did the LD50/30 increase indefinitely as overall exposure time was prolonged. The rapid phase of decay of radiation damage appeared to stop early, at 6 hours, after a single dose but not until after 18 hours of prolonged exposure.
International Journal of Radiation Biology | 1961
A.W. Law; R.H. Mole
Summary(1) As judged by changes in weight and DNA-content, the effects on the thymus of 50 r whole-body irradiation and of 50 r to the anterior half of the body were indistinguishable. This direct effect of radiation was not altered by adrenalectomy and was recovered from in five days.(2) Using the same criteria of effect, an abscopal effect on the thymus was demonstrated after 500 r to the posterior half of the body. The abscopal effect was at its greatest five days after irradiation and appeared to be due solely to a reduction in food-intake, since it could be almost exactly imitated by simple restriction of food-intake to the same level as that caused by the irradiation.(3) There was a curvilinear relation between thymic weight and body-weight. Adrenalectomy and food restriction altered this relation in opposite directions.
International Journal of Radiation Biology | 1959
R.H. Mole
Summary(1) A proper appreciation of ovarian damage by radiation is possible only if enough time is given for the damage to develop. Simple fertility is a less adequate measure of damage than reproductive capacity–the total number of young produced in the reproductive life-span. In C57BL mice this is halved by a single dose of 25 r of x-rays and by about 80 r of gamma-rays given at 2·2 r daily.(2) The high radiosensitivity of the ovary and the variation of somatic ovarian damage with dose-rate need to be taken into account when interpreting experimental results obtained in the female mouse, especially in studies of the effect of dose-rate on the frequency of radiation-induced mutations. It is possible that more attention should be given to somatic ovarian sensitivity when considering radiation hazards.
International Journal of Radiation Biology | 1968
E.V. Hulse; R.H. Mole; D.G. Papworth
SummaryThe observed incidence of epidermal and dermal tumours in mice following superficial external beta-irradiation may be accounted for by assuming that tumour induction is proportional to the square of the dose and that potential tumour cells lose their reproductive integrity according to a type C cell survival curve. n = 1·2 and D37 = 2440 rads for potential tumour cells of the epidermis and n = 1·9 and D37 = 2280 rads for potential tumour cells of the dermis.
International Journal of Radiation Biology | 1961
R.H. Mole; A.M. Thomas
SummaryFemale CBA mice were exposed to daily irradiation by gamma-rays or by fast neutrons at daily doses of from 3–50 rems for periods varying from four weeks to the duration of life. At daily doses between 3 and 30 rems, the mean survival-time reached a near minimum value after an exposure lasting less than half the duration-of-life exposure. Additional exposure had little further effect on survival-time.The shape of the mortality-curve depended systematically on the particular level of daily dose and on the duration of exposure, except possibly at the lowest daily dose. It is concluded that, if experimental support is to be sought for hypotheses relating life-span simply to dose or dose-rate, then experiments must be done with total doses of not more than a few hundred rems or with daily doses smaller than 3 rems.The shape of the curve relating total dose to mean survival-time in duration-of-life exposures can be accounted for on the assumption that all radiation damage is, in a mathematical sense, rep...
International Journal of Radiation Biology | 1966
D.W.H. Barnes; G.T. Bungay; R.H. Mole
SummaryDeaths between 25 and 275 days after mid-lethal x-irradiation were closely reminiscent of the ‘secondary disease’ of supralethally irradiated mice given allogeneic or xenogeneic cells. One-third of the mice with the diarrhoea syndrome died of it; the majority recovered spontaneously.The delayed mortality was prevented and diarrhoea minimized by treatment with 107 syngeneic lymph-node cells either soon after irradiation or 22 days later. Thus death from lymphoid insufficiency is a specific consequence of whole-body irradiation by mid-lethal doses. Radiation-induced somatic mutation in surviving cells may play a part.Early treatment with 5 × 106 syngeneic bone-marrow cells was also effective. Bone marrow at 22 days had less effect on diarrhoea and did not decrease mortality but changed the post-mortem findings, death occurring characteristically with markedly congested lungs and with amyloid deposits in spleen and liver.Body weight was increased but not restored to normal by treatment with either kin...
International Journal of Radiation Biology | 1966
R.H. Mole; D.G. Papworth
SummaryA re-analysis of already published data (Mandl 1959) shows that normal stage 1 oocytes of the young mature rat survived irradiation according to a typical exponential dose-response relation with D37 = 91 r and n = 2·3 ± 1·1. When the data for normal plus atretic oocytes are combined, the dose-response relationship for stage 1 is not simple. Oocytes at later stages of follicular development were very much more radioresistant.Large doses of radiation increased the proportion of atretic follicles in the earlier stages even as late as 30 days after exposure. In contrast at stages 5–6 doses of radiation too small to affect the number of normal oocytes reduced the number of atretic oocytes to levels much below those in unirradiated controls.
International Journal of Radiation Biology | 1962
G.J. Neary; E.V. Hulse; R.H. Mole
SummaryCBA mice have been irradiated from early maturity to death with low daily doses of fast neutrons or gamma-radiation delivered nearly continuously. For life-shortening the rbe of the fast neutrons was about 10 for mice of either sex; there was no significant dependence on size of daily dose within the range investigated.
International Journal of Radiation Biology | 1969
D.W.H. Barnes; R.H. Mole
SummaryA small number of allogeneic lymphoid cells may cause marked damage in recipients with depressed immune responsiveness, even when the antigenic differences are minor. Injection of 1000 C3H lymphoid cells into 9-month-old CBA mice irradiated with 750 rads increased mortality (a) in the second to sixth months and (b) after 18 months. In the first period there was a three-fold increase in syndromes attributable to lymphoid deficiency.Somatic mutation in lymphoid cells may be the explanation for delayed deaths during the second to sixth months following whole-body irradiation, when allogeneic cells have not been given.
International Journal of Radiation Biology | 1963
R.H. Mole
Data from recent studies of Sr/sup 90/ retention in mice on different dietary levels of P are reviewed. It is suggested that when long-term retention of Sr follows a power function, the magnitude of the exponent depends on the P content of the diet. (C.H.)