Biomedical subjects
D X Freedman
Publications and source records attributed to D X Freedman.
Tryptophan loading in hyperserotonemic and normoserotonemic adults.
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Violence (and a message for the 90s?)
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The search: body, mind, and human purpose.
Psychiatry's appropriate agenda and severe distractions in sustaining it are presently a concern and have historically been so as we struggle with the issues of linking body, mind, and human purpose. Biology requires behaving, variability, and the development of regulations to implement "purpose" in coping with the milieu. Psychiatry begins and ends with our patients--with their diseases and dysfunctions, their biographies and aspirations--which, as a clinical medical science, we must systematically study. Doing that, we will borrow from and pose problems for all the life sciences. New knowledge about how cells and biological systems acquire, code, and exchange information challenges all of medicine. In assessing our advances and future, we consider the history of biological issues in psychiatry and the "sins" of biologism or reductionism. We will see that research questions and strategies in the current study of disease and therapeutics have not fundamentally shifted from Freud and Meyer to modern molecular neurobiology. The tension between the socially conditioned purposive self and impersonal biological processes is an inescapable intrinsic tension for psychiatry of which we must be cognizant as we continue the search.
Pharmacology: policy implications of new psychiatric drugs.
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Of chairs and stools: or, what's academic about academic medicine?
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Will the real doctor please stand up?
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The President's Commission: realistic remedies for neglect. Pragmatic next steps--not a trip.
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Hyperserotonemia and amine metabolites in autistic and retarded children.
Mean whole blood serotonin (5-HT) levels were elevated in groups of autistic and severely retarded children. Eight of 27 (30%) individual autistic children, 13 of 25 (52%) severely retarded children, two of 23 (9%) mildly retarded children, and none of the control children had statistically significant blood 5-HT levels elevations (hyperserotonemia). Hyperserotonemic autistic children excreted more urinary 5-HT, 5-hydroxyindoleacetic acid (5-HIAA), tryptamine, and vanillylmandelic acid than did mildly retarded children with normal blood 5-HT levels. Rates of depletion and repletion of blood 5-HT levels in these two groups following reserpine therapy were identical. Oral tryptophan administration doubled urinary 5-HIAA excretion in both groups and raised urinary 5-HT levels in hyperserotonemic autistic children, but lowered urinary 5-HT in mildly retarded, normal blood 5-HT children. No clear mechanism for hyperserotonemia was found; the rationale for further investigations is discussed.
Vesicular and juxtavesicular serotonin: effects of lysergic acid diethylamide and reserpine.
An extensive analysis of subcellular serotonin (5-HT) compartmentation with and without reserpine was undertaken in order to localize further the effect of LSD on rat brain 5-HT. Modification of the subfractionation procedure resulted in an increase in purity of fractions and a decrease in variability of 5-HT content. With the modified procedure, the administration of LSD produced a significant increase in 5-HT in the nerve-ending fraction prepared from rat whole brain. LSD caused a 50% increase in 5-HT in the vesicular fraction which was recovered after osmotic disruption of nerve-endings. The increase of 5-HT in the vesicular fraction after LSD was not demonstrable in rats treated with reserpine for as long as 2 weeks postreserpine. Instead, with reserpine pretreatment the LSD-induced increase in 5-HT was localized to the intrasynaptosomally derived "end supernatant" as early as 48 hours postreserpine. Thus, an unanticipated "juxtavesicular" site capable of 5-HT retention or binding was detected. In crude subcellular fractions, by contrast, significant increase in 5-HT were not observed with LSD administration until 4 days after reserpine, at which time at least a 50% 5-HT repletion had occurred. This study of drug interactions suggests a juxtavesicular compartment that may be of functional importance in presynaptic binding or transport of 5-HT.
Editorial: The alma mater is smoking--this is dangerous to your health! Payoff and payback.
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Cardiovascular and subjective effects of intravenous cocaine administration in humans.
Nine volunteer subjects were tested with intravenously administered cocaine hydrochloride in doses ranging from 4 to 32 mg, as well as 10 mg of dextroamphetamine sulfate. Measures of cardiovascular and subjective effects were made. Generally parallel dose-effect functions were obtained for heart rate, blood pressure, Addiction Research Center Inventory scores, Profile of Mood Scales, and subject ratings. A substantial effect on each of these variables was recorded after 8 mg of cocaine. The increase continued and peaked at approximately 16 mg after which it usually leveled off. Ten milligrams of dextroamphetamine generally had an effect comparable to 8 to 16 mg of cocaine.
Rat brain aryl acylamidase: stereospecific inhibition by LSD and serotonin-related compounds.
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Stereospecific receptor sites for d-lysergic acid diethylamide in rat brain: effects of neurotransmitters, amine antagonists, and other psychotropic drugs.
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Plasma corticoids and brain tryptophan after acute and tolerance dosage of LSD.
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Smooth-pursuit eye movements, and diazepam, CPZ, and secobarbital.
This study examined the effects on smooth-pursuit eye tracking of single doses of CPZ (0.667 and 1.334 mg/kg), diazepam (0.071, 0.142, and 0.284 mg/kg), and secobarbital (100 mg). Only the barbiturate significantly affected the ability to follow a moving target with smooth-pursuit eye movements. In repeated testing of a single subject, 130 mg of secobarbital disrupted smooth-pursuit movements at least until 24 hrs after ingestion.