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Biomedical subjects

S D Morrison

Publications and source records attributed to S D Morrison.

At least 37 records · Page 2Linked to original sources
PubMed1982

Feeding response of tumor-bearing rats to insulin and insulin withdrawal and the contribution of autonomous tumor drain to cachectic depletion.

The Walker 256 carcinosarcoma growing in Sprague-Dawley rats and the Morris 5123 hepatoma growing in Buffalo rats both produce cachexia but have widely differing patterns of host metabolism and tumor growth. Both organisms respond to exogenous insulin with increased food intake and rate of weight gain of host. The insulin treatment response of food intake was 1.5 to 2 times and of body weight gain was 2 to 3 times that of tumor-free controls. Insulin does not accelerate tumor growth. On withdrawal of insulin, the reactive hypophagia seen in tumor-free rats does not occur in tumor bearers, and the host weight does not return to the expected untreated value as it does in tumor-free rats. Most of the weight gained during insulin treatment of tumor bearers above that gained by tumor-free rats is retained after withdrawal of insulin. A computer model based on the inference from these results, that the tumor-bearing host is blind to body weight error, indicates that this abnormality of feeding control could account for only about one-third of the observed depression of host weight and food intake.

Animals↗
PubMed1981

Histidine deficiency, food intake and growth in normal and Walker 256 carcinosarcoma-bearing rats.

Male Sprague-Dawley rats with and without growing Walker 256 tumors were fed 3 isonitrogenous, isoenergetic, semisynthetic diets. The N sources of the 3 diets were casein, a complete free amino acid mixture simulating casein, and the same amino acid mixture but now totally lacking histidine. Tumor-free rats and host and tumor components of tumor-bearing rats showed identical growth on the casein and on the casein-simulating free amino acid diets. Change from complete amino acid diet to histidine-free diet depressed food intake identically in controls and tumor-bearers in early stages of tumor growth. In later stages of tumor growth, when tumor-induced hypophagia had become apparent on the complete diet, the histidine-free diet had a progressively less depressive effect on food intake in the tumor-bearers.

Aging↗
PubMed1981

Cold-specific feeding response of rats to cold exposure and energy density of body weight change.

The increased food intake of rats exposed to cold is the result of increased intake due to cold (cold-specific compartment; A) and decreased intake due to simultaneously decreased body weight (weight-specific compartment; B). The two compartments are evaluated at 5, 13, and 17 degrees C. B is evaluated as the food intake of theoretical, isogravimetric control (identical to cold-exposed rats with respect to body weight and rate of change of body weight and identical to nonexposed rats in all other respects) that takes into account both the change in energy expenditure due to decreased body weight and the energy yield from tissue catabolism represented by change of body weight. A is the observed food intake minus B. A theoretical heat-flow model, in which expected changes in heat flow during cold exposure drive food intake to maintain or restore preexposure body weight status, corroborated the partition derived from experimental data. However, both the experimental results and the heat-flow model imply that the energy density of body weight change is negatively correlated with rate of body weight change. The energy density of weight change is high with high rates of weight loss and low with high rats of weight gain.

Animals↗
PubMed1981

Total parenteral nutrition in a methylcholanthrene-induced rat sarcoma model.

Problems with currently available studies of the effects of total parenteral nutrition (TPN) on rat tumor models include: inadequate definition of the natural history of the tumor model; use of nutritional techniques and solutions which have not been proven effective; failure to allow animals to recover from stress of catheterization before starting nutritional manipulation; short-term studies; failure to use sham-operated orally fed control animals; and inadequate evaluation of nutritional result. We have instituted TPN after a 4-day postcatheterization recovery period in a defined methylcholanthrene-induced rat sarcoma model. Preliminary results suggest that TPN increases tumor weight without changing tumor composition of water, nitrogen, or fat. TPN also increases carcass fat and water content, but not carcass protein. In tumor-bearing animals, the percentage of energy expended on activity decreases with increasing tumor burden in both TPN and orally fed controls. TPN in these studies appears to support fat stores and stimulate tumor growth.

Animals↗
PubMed1981

Control of food intake in experimental tumor growth.

The cachectic depletion of cancer is invariably an immediate consequence of progressive deficit of food intake below metabolic cost. The deficit of food intake arises from successive impairment of individual feeding controls. The impairment of some feeding controls well before there is overt hypophagia or cachexia indicates that overt cachexia is preceded by a silent or compensated cachectic process, and behavioral compensation for deteriorating feeding controls can be demonstrated. The hypothalamic components of control of food intake are not affected. In some instances, severe asthenic reduction in motor activity further disables capacity to feed since feeding is a motor activity and motor capability is a necessary condition for feeding. The variability in timing and severity of cachectic decay among different tumors and individuals is a function of the timing and sequencing of breakdown of individual controls, capacity for compensation, and impairment of motor capability, and the extent to which all possible controls are functionally expressed in the normal individual.

Animals↗
PubMed1981

Extrahypothalamic mediation of changes in feeding behavior induced by growth of Walker 256 carcinosarcoma in rats.

Feeding efficiency (amount of food ingested per unit of feeding activity) was chronically depressed in male Sprague-Dawley rats recovered from the acute aphagia or hypophagia of lateral hypothalamic damage. The extent of depression varied with the severity of the acute feeding response to hypothalamic damage. Growth of Walker 256 carcinosarcoma in intact rats increased feeding efficiency. Chronic lateral hypothalamic damage did not significantly attenuate tumor-induced increase in feeding efficiency but lowered the initial and maximum efficiency levels. Growth of the tumor-bearing host was depressed by residual lateral hypothalamic damage, but this depression was not related to the severity of the acute feeding response to damage.

Animals↗
PubMed1980

Protein quality, food intake and growth in normal and Walker 256 carcinosarcoma-bearing rats.

The effect of supplementation of dietary gluten with its first and second limiting amino acids (lysine and threonine) on food intake and growth was examined in normal and Walker 256 carcinosarcoma-bearing male, Sprague-Dawley rats. Two diets were used. Diet G had 16.4% gluten and diet GLT had (%): gluten 15, L-lysine.HCl 1, and L-threonine, 0.4 Normal and tumor-bearing animals (7) were fed each diet from day 7 until day 20 post-transplant of the tumor bearers. Food intake in the tumor-bearers was lower than that of controls (P < 0.01) from day 10 post-transplant. Normal animals fed diet GLT ate more than those fed diet G throughout the experiment. A similar effect of protein quality on the food intake of tumor-bearers was seen until day 15 post-transplant; thereafter, food intake of tumor-bearers was similar on both diets. Tumor-bearing animals had lower (P < 0.01) protein and lipid contents than controls on both diets. Diet had no effect on tumor weight or content of protein, lipid, DNA or RNA. Protein and lipid contents of hosts and controls on diet GLT were higher (P < 0.5) than for their counterparts on diet G.

Animals↗
PubMed1977

Retrospective audit: depressive neurosis.

The charts of 100 patients with a primary diagnosis of depressive neurosis were subjected to retrospective audit using a format adapted from the American Psychiatric Association's Model Criteria Sets. Nineteen of the 33 unjustified variations from the audit criteria involved variations from the 8-28 day length of hospital stay. The author raises the question of whether the lower limit of 8 days is sufficiently flexible to permit hospitalization of acutely suicidal patients who can be discharged to outpatient care in less than 8 days.

Adjustment Disorders↗
PubMed1977

The hypothalamic syndrome in rats.

The original conception of the hypothalamus controlling feeding by the activity of two specific and reciprocally inhibitory centers has now been largely abandoned. Detailed neural research using a wide variety of methods has demonstrated the complex morphological and functional organization of this part of the brain and has modified the earlier simplistic approach. However, examination of the feeding responses to a variety of stimuli that represent components of control of feeding indicates that much or even most feeding control is extrahypothalamic. As demonstrated by the obesity or aphagia resulting from hypothalamic damage or from reversible hypothalamic interference, the hypothalamus influences or modulates feeding control, possibly by an enabling action, but it does not itself substantially control food intake either in the short or the long term. In the cachaxia of cancer, which can tentatively be regarded as a negative obesity, and which is closely reproducible in a rat model, the decline of food intake can be attributed to failure of control components that are all extrahypothalamic, and the deterioration of control of feeding appears to be quite independent of the hypothalamus. The very detailed reconstruction of intrahypothalamic circuitry that has been developed in recent years has not yet had any real impact on the problem of where or how the active control of food intake is generated or the way in which the hypothalamus influences this control.

Animals↗
PubMed1976

Generation and compensation of the cancer cachectic process by spontaneous modification of feeding behavior.

Daily food intake and corresponding feeding activity (measured as duration) and feeding efficiency (amount of food ingested per unit of feeding activity) were measured both in normal Sprague-Dawley and Buffalo rats and during growth of Walker 256 and 4M mammary carcinomas in Sprague-Dawley rats and of Morris 5123 hepatoma in Buffalo rats. Estimates of meal size and frequency were also obtained. Growth of the carcinomas produced a decline in feeding activity accompanied, early in tumor growth, by a compensatory increase in feeding efficiency with no resultant effect on food intake. This compensated decline in feeding activity was due to reduction in average meal duration. Later, meal frequency was also reduced, with further reduction in feeding activity and reduction in food intake. There was little change in average meal size. The hepatoma produced a different detailed pattern of effect on feeding behavior. These effects are not nonspecific reactions to foreign tissue. The effects imply behavioral compensation for the breakdown of a rapidly responding physiological control of food intake and can be interpreted in terms of successive impairment of feeding control mechanisms that have different response rates and different behavioral modes.

Animals↗
PubMed1975

Origins of nutritional imbalance in cancer.

Some parallels and differences are considered between the nutritional circumstances that favor carcinogenesis and those that favor tumor growth and host cachexia. From evidence on deletion of physiological feeding controls and changes in feeding behavior during tumor growth and from evidence on differences in sets of available feeding controls and in feeding behavior among normal individuals, it is suggested that acquisition of possibly carcinogenic dietary habits may originate, in part, from innate deficits in physiological feeding controls.

Animals↗
PubMed1975

Aggression in adolescents: Use of the Buss-Durkee Inventory.

The Buss-Durkee Inventory (BDI) is a 75-item true-false design to measure hostility and aggression. Norms have been established for adult populations, and data are available for adult psychiatric populations. Adolescent norms have not been established, nor are data available for adolescent psychiatric populations. This study provides BDI data on 438 high school students, giving breakdown by age, sex, and race. In addition, BDI scores for 100 patients admitted consecutively to an adolescent inpatient unit are presented. Scores on the BDI were higher in the younger high school age groups. Female patients had higher scores than girls in the high school control group; male patients scored lower than their male controls. Female patients surprisingly scored higher than male patients.

Adolescent↗