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Biomedical subjects

R C Albucher

Publications and source records attributed to R C Albucher.

5 recordsLinked to original sources
PubMed1998

Defense mechanism changes in successfully treated patients with obsessive-compulsive disorder.

OBJECTIVE: Changes in defense mechanisms after treatment of patients with obsessive-compulsive disorder (OCD) were measured by using an established rating scale. METHOD: Before and after 7-week group behavior therapy, 17 patients with DSM-III-R OCD were assessed with the Defense Style Questionnaire, Yale-Brown Obsessive Compulsive Scale, and Beck Depression Inventory. RESULTS: After behavior therapy the patients evidenced significant decreases in Yale-Brown Obsessive Compulsive Scale scores and significant increases in the use of more adaptive defense mechanisms. There were no significant changes in three maladaptive defense mechanism categories. The improvement in adaptive defenses was independently linked to improvement both in OCD and in depression. CONCLUSIONS: Personality as defined by defense mechanisms may be more amenable to brief behavioral treatment than previously thought. The permanence of these changes must be further assessed.

Adult↗
PubMedDate not supplied

Normal levels of hepatic drug-metabolizing enzymes in neonatally induced, growth hormone-deficient adult male and female rats.

The effects of chronic growth hormone deficiency on the growth hormone-dependent, sexually dimorphic hepatic drug-metabolizing enzymes were studied in adult rats of both sexes. Neonatal administration of monosodium L-glutamate produced the expected syndrome characterized by stunted growth, obesity, prolonged vaginal estrus, and an inhibition in the growth of the pituitaries, adrenals, gonads, sexual accessory organs, and kidneys. Associated with these abnormalities was a 90% reduction in the concentration of serum growth hormone in male and female rats. In contrast, the activities of hepatic aniline hydroxylase, total cytochrome P-450, and the Michaelis constants and maximal velocities for hexobarbital hydroxylase and UDP-glucuronosyltransferase were unaffected by the profound deficiency in growth hormone.

Animals↗