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Showing papers in "Science in 1958"


Journal Article•DOI•
28 Feb 1958-Science

635 citations





Journal Article•DOI•
James L. Olds1•
14 Feb 1958-Science
Abstract: My conclusions are these: (i) The cells which mediate primary rewarding effects are located in a midline system running from the midbrain through the hypothalamus and midline thalamus and into the subcortical and cortical groups of the rhinencephalon. (ii) The cell groups which mediate primary rewarding effects are different from those which mediate primary punishing effects. (iii) Despite this relative independence, there are, undoubtedly, relationships of mutual inhibition existing between these two systems. Rewards do, among other things, tend to reduce sensitivity to pain, and punishments do tend to reduce rewarding effects. (iv) These primary reward systems of the brain are subdivided into specific drive-reward subsystems mediating the specific drives such as hunger and sex. (v) Because there are also subsystems of this set of rewarding structures sensitive to different chemical effects, it is reasonable to hope that eventually it will be possible to control the reward systems pharmacologically in cases where behavior disorders seem to result from deficits or surfeits of positive motivation.

353 citations



Journal Article•DOI•
19 Dec 1958-Science
TL;DR: The results indicate that the genetic hazards, at least under some radiation conditions, may not be as great as those estimated from the mutation rates obtained with acute irradiation, however, it should not be forgotten that even the lower mutation rates obtaining with the present intensity levels are still appreciable.
Abstract: New data have clearly confirmed the earlier finding that specific locus mutation rates obtained with chronic gamma irradiation of spermatogonia are lower than those obtained with acute x-rays. Since this result is in contrast to classical findings for Drosophila spermatozoa, and apparently contradicts one of the basic tenets of radiation genetics, it was important to determine what factors were responsible for it. Experiments undertaken for this purpose reveal the following: (i) the lower mutation frequency is due mainly to difference in dose rate of radiation, rather than quality; (ii) a dose-rate effect is not obtained in experiments with mouse spermatozoa, confirming classical findings for spermatozoa, and indicating that the explanation for intensity dependence in spermatogonia resides in some characteristic of gametogenic stage; and (iii) a dose-rate effect is found not only in spermatogonia but also in oocytes, where cell selection is improbable, indicating that the radiation intensity effect is on the mutation process itself. A threshold response for all mutations in spermatogonia and oocytes is not a necessary consequence of the findings. Plausible hypotheses consistent with the present results can lead to other predictions. From a practical point of view, the results indicate that the genetic hazards, at least under some radiation conditions, may not be as great as those estimated from the mutation rates obtained with acute irradiation. However, it should not be forgotten that even the lower mutation rates obtained with the present intensity levels are still appreciable (16).

322 citations


Journal Article•DOI•
04 Apr 1958-Science

283 citations



Journal Article•DOI•
14 Nov 1958-Science
TL;DR: Electronic averaging of potentials recorded from the human scalp reveals the presence of small average responses following the presentation of click stimuli and it is suggested that the short-latency components of these responses are cortical in origin.
Abstract: Electronic averaging of potentials recorded from the human scalp reveals the presence of small average responses following the presentation of click stimuli. These responses are first detectable near the subject's psychophysical threshold and vary in amplitude with click intensity. It is suggested that the short-latency components of these responses are cortical in origin.

256 citations


Journal Article•DOI•
Fritz Lipmann1•
12 Sep 1958-Science














Journal Article•DOI•
12 Sep 1958-Science
TL;DR: Evidence is presented which indicates that the principal pathway of metabolism of epinephrine in man is O-methylation to metanephrine, a physiologically inactive compound, and that the enzyme responsible for this reaction, catechol-O-methyl transferase, is the enzyme mainly involved in the termination of action in man.
Abstract: Evidence is presented which indicates that the principal pathway of metabolism of epinephrine in man is O-methylation to metanephrine. The extent of the conLversion to metanephrine, a physiologically inactive compound, indicates that the enzyme responsible for this reaction, catechol-O-methyl transferase, is the enzyme mainly involved in the termination of action of epinephrine in man.