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Taraxein-like ExtractsEffects on Rat Behavior
JOHN R. BERGEN, PhD;
FREDERIC W. GRAY, MD;
ROBERT B. PENNELL, PhD;
HARRY FREEMAN, MD;
HUDSON HOAGLAND, PhD
Arch Gen Psychiatry. 1965;12(1):80-82.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings. |
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From previous collaborative studies with the Worcester State and Medfield State Hospitals and the Protein Foundation, we have reported evidence for a taraxein-like substance found in human plasma proteins which may be related to schizophrenia.1,2 The plasma factor has been shown to disturb the performance of trained rat behavior to a significantly greater degree when derived from the blood of schizophrenic patients than from the blood of psychotic nonschizophrenic individuals or from normal persons. The factor may be a concomitant of disease or stress processes so plasma factor titers were investigated in physically ill persons without psychiatric disorders to settle this point.
Methods
Nonpsychotic donors for the study were patients of the Rutland Heights VA Hospital selected from the following categories: (1) tuberculosis, (2) carcinoma, (3) chronic hospitalization, and (4) post-operative. Collections from psychotic individuals were obtained at the Medfield and Worcester State Hospitals primarily
. . . [Full Text PDF of this Article]
Author Affiliations
SHREWSBURY, MASS; RUTLAND, MASS; BOSTON; MEDFIELD, MASS; SHREWSBURY, MASS
Senior Scientist, Worcester Foundation for Experimental Biology (Dr. Bergen); Chief of Surgery, Rutland Heights VA Hospital (Dr. Gray); Director, Protein Foundation (Dr. Pennell); Director of Research, Medfield Foundation (Dr. Freeman); Co-Director, Worcester Foundation for Experimental Biology (Dr. Hoagland).
Present address (Dr. Gray): Department of Surgery, Veterans Administration Center, Kecoughtan, Va.
Fenwal Laboratories, Morton Grove, Ill.
Footnotes
Submitted for publication Aug 5, 1964.
Preliminary report read before the Meeting of the Federation of American Societies for Experimental Biology, April 1964, Chicago.
This study was supported in part by Public Health Service Research grant No. MH 02967 from the National Institute of Mental Health and by grants from the Scottish Rite Committee on Research in Schizophrenia, and the Ittleson Family Foundation.
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