Domestic animal visitation as therapy with adult home residents.
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Biomedical subjects
Publications and source records attributed to S B Johnson.
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Patterns of polyunsaturated fatty acids of serum phospholipids were measured for groups of alcoholics without cirrhosis, alcoholics with cirrhosis, cirrhotics without alcoholism, and a control population. Alcoholics without cirrhosis showed increased polyunsaturated fatty acids derived from linoleic and linolenic acids, but in cirrhotics these products were decreased. Alcoholism accentuated the abnormal polyunsaturated fatty acid pattern of cirrhosis. In alcohol abuse without cirrhosis, the level of 20:3 omega 9 (20 acyl carbon atoms:3 double bonds, omega, 9 carbon atoms beyond last double bond) was significantly increased, despite adequate levels of linoleic and arachidonic acids. Liver involvement appears necessary for development of deficiencies of polyunsaturated fatty acids in serum phospholipids, of which arachidonic acid deficiency is of the largest magnitude.
Fifteen serum samples from 11 women with preeclampsia and 19 samples from 10 normal third-trimester pregnancies were analyzed for total nonesterified fatty acids and total nonesterified arachidonic acid. The percentages of arachidonic acid in nonesterified fatty acids, in phospholipids, in triglycerides, and in cholesterol esters were also measured in each sample. The same analyses were done on serum from six samples of cord blood from each group. Cord blood sera from preeclamptic and normal pregnancies had much less total nonesterified fatty acids than the corresponding maternal sera but had much higher percentages of arachidonic acid in each of the major lipid categories. The maternal phospholipids and cholesterol esters had higher proportions of arachidonic acid in preeclampsia than in normal pregnancy. Samples from placentas of preeclamptic pregnancies had significantly lower proportions of arachidonic acid in the nonesterified fatty acids and triglycerides than normal placentas. These findings suggest a decreased availability of arachidonic acid in the fetal circulation which may result in decreased production of prostacyclin in preeclampsia.
The Family Adaptability and Cohesion Evaluation Scales (FACES), a measure of family functioning, contains three scales: cohesion, adaptability, and social desirability. These were slightly modified (FACES-R) on the basis of pilot data and were administered to 42 clinic families (families seeking or receiving psychological services) and 206 nonclinic families. Support for the scales was found in high coefficient alpha reliabilities and similarity of the sample means and standard deviations to those of the standardization sample. However, there was little agreement among family members' scale scores. Therapists' ratings of cohesion and adaptability did not correlate with scale scores among clinic families. There was no difference between clinic and nonclinic samples on the cohesion or adaptability scales, although the social desirability scale did discriminate between groups. Factor analysis suggested that cohesion, adaptability, and social desirability cannot be clearly differentiated using this measure.
The effects of biotin and protein-calorie deficiency on metabolism of liver phospholipids in rats were determined. Weanling male Long-Evans rats were fed ad libitum a biotin-deficient (0.4 micrograms biotin/g diet) or a biotin-adequate (2.4 micrograms biotin/g diet) diet for 49 days. A pair-fed group was fed biotin-adequate diet but restricted to the amount consumed by biotin-deficient rats. The effects of these diets on food intake, weight gain, biotin content of serum and fatty acid composition of liver phospholipid were determined. Growth and food intake were significantly depressed in biotin-deficient and pair-fed rats. Biotin concentration in serum was significantly reduced in biotin-deficient and in pair-fed rats. Biotin deficiency caused significantly increased concentrations of 15:0, 17:0 and total odd-chain fatty acids in liver phospholipids. Combined biotin and protein-calorie deficiency and protein-calorie deficiency alone caused significantly increased concentrations of 18:2 omega 6 in liver phospholipids. Biotin deficiency caused significant reduction in liver phospholipid 20:3 omega 6. Reduced arachidonic acid (20:4 omega 6) level was due to combined biotin protein-calorie deficiency. Protein-calorie deficiency alone was primarily responsible for reduced levels of 22:5 omega 6. Biotin deficiency alone caused significant increases in liver phospholipids 18:3 omega 3 and 22:6 omega 3.
The influence of reduced food intake on metabolism of liver phospholipids (PL) in zinc-deficient (ZD) rats was measured. Wealing male Long-Evans rats were fed ad libitum zinc-deficient (2 micrograms Zn/g diet) and zinc-adequate (20 micrograms Zn/g diet) diets for 21 days. A pair-fed (PF) group was included. ZD and PF rats displayed significantly increased levels of linoleic (18:2 omega 6) and dihomo-gamma-linolenic acid (20:3 omega 6). Both ZD and PF rats displayed increased levels of gamma-linolenic acid (18:3 omega 6), but the increase was significant only in PF rats. ZD and PF rats displayed decreased levels of arachidonic acid (20:4 omega 6), but the decrease was significant only in PF rats. Both ZD and PF rats displayed significantly reduced levels of 22:5 omega 6. Both ZD and PF rats displayed increased products of delta 6 desaturation and decreased products of delta 5 and delta 4 desaturation. Significantly increased products of delta 9 desaturation were noted in both ZD and PF rats. ZD and PF rats displayed significant increases in C20 elongation products. ZD and PF rats displayed significantly decreased levels of omega 6 metabolites but not total omega 6 acids. ZD rats showed significantly increased levels of total omega 3 acids and omega 3 metabolites. ZD and PF rats showed significant increases in omega 9 acids but not significant changes in omega 9 metabolites. This study does not indicate that zinc affects the delta 6 desaturase in the metabolism of essential fatty acids. The aberrations previously attributed to zinc deficiency are probably due to the accompanying decreased food intake.
Fatty acid compositions of phospholipids of heart, liver, kidney, aorta, and serum from rats having streptozotocin-induced diabetes were determined and compared with those of nondiabetic controls. Linoleic and dihomo-gamma-linolenic acids were increased whereas arachidonic acid was decreased in most tissues, suggesting an impairment of delta 5-desaturase activity. Acids derived from linolenic acid were increased in some diabetic tissues from diabetic animals although the linolenic content was normal, indicating less impairment in the desaturation of the omega 3 series of fatty acids. Diabetes suppressed all polyunsaturated acids in the whole animal, but the competition between omega 3 and omega 6 acids favored the excessive suppression of long-chain omega 6 acids and an increase in the proportion of omega 3 acids in lipids of vital tissues. These changes in fatty acid composition of the phospholipids may have significant effects on cellular functions and vasoregulatory control mechanisms in diabetes.
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This study assessed change in the frequency of primary nocturnal enuresis as produced by either behavioral conditioning with a urine alarm, pharmacotherapy with imipramine hydrochloride, or assignment to a clinical waiting list. The study also investigated the effect of treatment method and outcome on subjects' level of emotional and behavioral adjustment. An attempt was made to identify pretreatment predictors of treatment outcome and premature withdrawal from the treatment program. The results indicated a significantly more effective outcome for the conditioning approach. Comparison of pre- and post-treatment measures of adjustment provided insufficient evidence to support the hypotheses that either change in the frequency of nighttime wetting or the method of treatment received would influence the subject's level of emotional and behavioral adjustment. The enuresis tolerance scale was found to be a highly significant predictor of early termination from conditioning treatment.
Fatty acid patterns of the serum lipids were measured in 17 children with Reye's syndrome (RS). Serial measurements of total serum free fatty acids (FFA) showed that levels were increased during RS and, after recovery, were significantly lower in the patients who survived. Fatty acid patterns of serum FFA, triglycerides, and phospholipids in patients with RS were significantly different from those in controls. In RS the polyunsaturated fatty acid content of phospholipids was less than control values; in the FFA, it was higher. This was consistent with the possible involvement of increased phospholipase activity. The increase in polyunsaturated fatty acids in FFA, the precursors of prostaglandins, suggests that a grossly disturbed prostaglandin pattern may occur in RS. These changes in lipid metabolism may be related to the abnormal hepatic and neurological functions observed in RS.
Rats were fed purified diets containing (i) partially hydrogenated soybean oil as source of isomeric octadecenoic acids, (ii) hydrogenated coconut oil as source of saturated fatty acids, and (iii) a low level of corn oil as low-fat control. All diets contained 18% of the linoleate requirement. Rat liver and heart phospholipids were analyzed by gas/liquid chromatography for fatty acids, and liver, microsomes were assayed for desaturase (acyl-CoA, hydrogen-donor: oxidoreductase, EC 1.14.99.5) activities. Products of desaturation reactions measured analytically provided more information with greater statistical significance than did the enzymatic assays. Rats fed isomeric octadecenoic acids showed more severe essential fatty acid deficiency than did saturated-fat and control groups. The suppression of linoleate metabolites was largely due to decreased delta 5 and delta 6 desaturase activities. At several levels of linoleate, the deficiency was more severe at the higher level of isomeric octadecenoic acids. Increasing the intake of linoleate to 7.5% of calories did not suppress deposition of isomeric unsaturated acids in tissue lipids.
A 6-yr-old girl who lost 300 cm of intestine was maintained by total parenteral nutrition. After 5 months on a preparation rich in linoleic acid but low in linolenic acid she experienced episodes of numbness, paresthesia, weakness, inability to walk, pain in the legs, and blurring of vision. Diagnostic analysis of fatty acids of serum lipids revealed marginal linoleate deficiency and significant deficiency of linolenate. When the regimen was changed to emulsion containing linolenic acid neurological symptoms disappeared. Analysis indicated that linoleate deficiency had worsened but linolenate deficiency had been corrected. The requirement for linolenic acid is estimated to be about 0.54% of calories.
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The aim of the present study was to examine the fatty acid patterns of plasma phospholipids, cholesteryl esters, triglycerides and free fatty acids in patients with Sjögren-Larsson syndrome in order to detect whether absorption or metabolism is essential fatty acids may be abnormal. The fatty acid patterns were analyzed by gas liquid chromatography. The proportions of 23 fatty acids were calculated. The parameters used for assessment of the essential fatty acid metabolic status were calculated and compared with those from a group of institutionalized mentally retarded patients and from a group of healthy controls. There was no significant difference in either the fatty acid components or parameters used to evaluate the essential fatty acid metabolic study when the mentally retarded and control groups were compared. The relative concentration of linoleic acid (18:2 omega 6) in plasma phospholipids in patients with Sjögren-Larsson syndrome did not differ significantly from that of the healthy or mentally retarded controls, indicating that the Sjögren Larsson syndrome does not involve a dietary essential fatty acid deficiency or a defect in absorption of linoleate. In the phospholipids of Sjörgren-Larsson syndrome patients, the metabolites derived from linoleic acid were found to be significantly lower than in health controls, suggesting the metabolic defect. The total products of delta 6 desaturation were reduced to 3% of that in controls, whereas the products of delta 5 and delta 9 desaturation were not noticeably affected in the patients with Sjögren-Larsson syndrome. All individuals with Sjörgren-Larsson syndrome exhibited decreased products of delta 6 desaturation which also affected subsequent metabolites in the metabolite sequence.
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A dermatoglyphic study of 197 adult Caucasian males with a confirmed diagnosis of epilepsy was carried out in an attempt to ascertain possible associations between aberrant dermatoglyphic and seizures and to estimate their diagnostic usefulness. Qualitative and quantitative fingertip and palmar dermatoglyphic traits were evaluated. The data were analyzed by etiology seizures. Previous studies and our own earlier data (Schaumann 1979) analyzed by univariate statistical methods indicated the presence of some dermatoglyphic deviations in patients with epilepsy, suggesting the existence of a genetic predisposition to seizures of various etiologies. In the present study, a multivariate analysis was employed on an enlarged patient sample. Three variables were found to be significant: an increased main line index on the right palm (p less than .01) and decreased a-b ridge counts on both left and right palms (p less than .001). Tests of the eigenvalues showed only one value to be significant and accounting for 71.8% of the intergroup variation.