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Biomedical subjects

M Fields

Publications and source records attributed to M Fields.

At least 91 records · Page 5Linked to original sources
PubMed1986

Female rats are protected against the fructose induced mortality of copper deficiency.

Experiments were conducted in copper deficient male and female rats fed diets containing fructose or starch in order to determine whether the same type of interaction between copper status and dietary carbohydrate found in male rats also occurs in the female rat. Mortality occurred only in the male rats fed the fructose diet deficient in copper with 40% of the animals dying during the 8 week study. Only anemia, hypercholesterolemia, increased BUN, heart hypertrophy and reduced body weight were observed in these animals which could be related to their mortality. Despite the increased mortality, plasma ceruloplasmin, erythrocyte SOD and hepatic copper concentrations were reduced to a similar extent in all rats regardless of the sex of the animals or of the type of dietary carbohydrate fed. The results of the present study indicate that although direct measurements of copper status of female rats fed fructose diet deficient in copper are similar to their male counterpart, they are apparently protected from the lethal consequences of the deficiency.

Anemia↗
PubMed1985

Parameters and the analytic process: a contribution to the theory of the "mature transference".

This case presentation deals with a patient whose preoedipally and oedipally determined deficit in directing libido and aggression toward the world, and resulting resistance to the analytic process, required the use of a "reducible" parameter designed to help him harness libido and aggression in the service of intellectual interest. The peculiar conformation of the patient's Oedipus complex, superimposed on a developmental deficit, led to profound resistance to genetic oedipal and preoedipal interpretations of the paternal and maternal transferences, respectively. The resistance took the form of an avowed lack of intellectual interest in the analytic work which paralleled his lack of interest both in his career and in his interpersonal relationships. The use of a technical parameter involving the provision of advice on an issue of pressing concern and a subsequent "preinterpretive enactment" dealing with the nature of psychoanalytic interpretation were instrumental in securing a "mature transference" (Stone, 1961) and in controlling the resistance-based regression. Via the instrumentality of the parameter, the case provides a concrete exemplification of Kanzer's (1975, p. 49) claim that "even the patient's antagonism toward therapy. . . may play a constructive part in the treatment."

Adult↗
PubMed1985

Effects of different dietary carbohydrates on hepatic enzymes of copper-deficient rats.

The present study was undertaken to measure the activities of several hepatic enzymes of regulatory importance in the pathways of lipogenesis and gluconeogenesis in rats fed diets marginally deficient in copper (1.2 micrograms Cu/g of diet) and containing either fructose, glucose, or starch as the carbohydrate sources. Although all copper-deficient rats exhibited the characteristic signs of copper deficiency, they were more pronounced in rats fed the diet containing fructose. Except for the activity of phosphoenolpyruvate carboxykinase which was unaffected either by copper deficiency or by the type of dietary carbohydrate, the hepatic activities of glucose-6-phosphate dehydrogenase, malic enzyme, L-alpha-glycerophosphate dehydrogenase and fructose 1,6-diphosphatase were unaffected by copper deficiency but were affected by the type of carbohydrate in the diet. Fructose produced the greatest increase in enzymatic activities, whereas starch produced the least activity and glucose induced an intermediate effect. These results indicate that the deleterious effects of a fructose diet deficient in copper on biochemical and physiological indices could not be due to an immediate metabolite of fructose. However, the involvement of a subsequent metabolite of fructose in the mechanism of copper utilization and/or requirement cannot be excluded.

Animals↗
PubMed1984

Effect of dietary carbohydrates and copper status on blood pressure of rats.

Copper deficiency was induced in rats by feeding diets containing either 62% starch, fructose or glucose deficient in copper for 6 weeks. All copper deficient rats, regardless of the dietary carbohydrate, exhibited decreased ceruloplasmin activity and decreased serum copper concentrations. Rats fed the fructose diet exhibited a more severe copper deficiency as compared to rats fed either starch or glucose. The increased severity of the deficiency was characterized by reduced body weight, serum copper concentration and hematocrit. In all rats fed the copper adequate diets, blood pressure was unaffected by the type of dietary carbohydrate. Significantly reduced systolic blood pressure was evident only in rats fed the fructose diet deficient in copper. When comparing the three carbohydrate diets, the physiological and biochemical lesions induced by copper deprivation could be magnified by feeding fructose.

Animals↗
PubMed1984

The interaction of type of dietary carbohydrates with copper deficiency.

The present study was designed to determine if the more severe copper deficiency in rats fed sucrose and fructose, as compared to starch, is due to a specific effect of the fructose or to a nonspecific effect of any simple carbohydrate. Seventy weanling male rats were fed, for 9 wk, copper-deficient diets or copper-supplemented diets containing either 62% starch, fructose, or glucose. Decreased hematocrit, serum copper, and ceruloplasmin concentrations but increased heart and liver weights, total liver lipid, and hepatic iron concentrations were found in all copper-deficient rats regardless of the dietary carbohydrate. Feeding rats the high glucose diet decreased plasma albumin and liver glycogen but increased blood urea nitrogen when compared to rats fed starch. However, rats fed fructose generally exhibited a more severe copper deficiency as compared to rats fed either starch or glucose. The severity was characterized by lower (p less than 0.05) body weight, liver glycogen, hematocrit, serum copper, and albumin. Conversely, liver and heart weights, blood urea nitrogen, and plasma glutamic oxaloacetic transaminase were higher (p less than 0.05). Plasma cholesterol was increased by copper deficiency only in rats fed fructose or glucose. During the study, 17 of the 40 rats fed copper-deficient diets died; 66% of those fed fructose, 26% fed glucose, and 30% fed starch. These results suggest that the fructose moiety of sucrose is responsible for the increased severity of copper deficiency in rats fed sucrose as compared to starch.

Animals↗
PubMed1984

Impairment of glucose tolerance in copper-deficient rats: dependency on the type of dietary carbohydrate.

Copper deficiency was induced in weanling rats in order to study the possible interaction between the types of dietary carbohydrate and copper deficiency on glucose tolerance. Weanling male rats were fed copper-deficient or copper-supplemented diets containing either 62% starch, fructose or glucose. During week 5 the fructose portion of the copper-deficient diet was replaced (20 rats) by starch (10 rats) or glucose (10 rats). During the 9th week, an oral glucose tolerance test weas performed. Copper deficiency was associated with impaired glucose tolerance characterized by increased blood glucose and decreased insulin levels only in copper-deficient rats fed the monosaccharides fructose or glucose but not the polysaccharide starch. Changing the dietary carbohydrates in the copper-deficient diet from fructose to starch increased insulin levels and decreased blood glucose in response to the glycemic stress when compared to rats continuously fed fructose. Although both glucose and fructose feeding impaired the glucose tolerance, fructose was more diabetogenic. This could be demonstrated by some improvements in glucose tolerance when the copper-deficient rats were switched from the fructose to the glucose diet. The data indicate that copper deficiency per se does not impair glucose tolerance.

Animals↗
PubMed1984

The severity of copper deficiency in rats is determined by the type of dietary carbohydrate.

The purpose of this investigation was to study the interaction between copper and dietary carbohydrates on clinical and enzymatic indices associated with copper deficiency. Copper deficiency was produced in rats by feeding diets adequate in all nutrients including selenium and chromium, but marginal in copper (1.2 micrograms/g diet) containing 62% of either starch, fructose, or glucose. During the fifth week, the fructose of the copper-deficient diet (20 rats) was replaced by either starch (10 rats) or by glucose (10 rats). The experiment was terminated after 11 weeks. Copper deficiency in rats fed fructose significantly lowered body weight and hematocrit, but increased liver weight, blood urea nitrogen, ammonia, cholesterol, and triglycerides when compared to rats fed starch or glucose. The copper metalloenzyme, superoxide dismutase, the selenoenzyme, glutathione peroxidase, and hepatic ATP were decreased in the copper-deficient rats fed fructose as compared to copper-deficient rats fed starch or glucose. These results indicate that fructose may be the dietary component which has a deleterious effect on copper and selenium status. Changing the type of dietary carbohydrate in copper-deficient rats from fructose to either starch or glucose ameliorated the severity of the deficiency. The protective effects were more pronounced with starch than with glucose.

Adenosine Triphosphate↗
PubMed1983

Role of dietary fructose in the enhancement of mortality and biochemical changes associated with copper deficiency in rats.

Rats were fed copper deficient (0.9 microgram/g) or copper-supplemented diets in which the carbohydrate was either starch, sucrose, or fructose (62% by weight) for 7 wk. Regardless of the nature of the carbohydrate, copper deficiency decreased blood ceruloplasmin activity, hepatic copper and ATP levels, and increased plasma cholesterol and triglycerides. Copper deficiency in rats fed sucrose or fructose, but not those fed starch, significantly lowered blood hematocrit, Hb, and albumin and significantly increased heart and liver weight and the glucose response to a glycemic stress. Hepatic copper level was significantly lower in copper-deficient rats fed sucrose or fructose than in those fed starch. Fasting blood glucose, cholesterol, and triglyceride levels were significantly higher in copper deficient rats fed fructose than in those fed starch. During the study 14 copper-deficient rats died, one of 10 fed starch, six of 20 fed sucrose, and seven of 20 fed fructose. Death was apparently the result of rupture of the heart in the region of the apex. These results indicate that fructose-containing carbohydrates as compared to starch markedly increase the severity of copper deficiency in rats. Whether this effect is due to differences in the nature of the simple carbohydrate (fructose versus glucose) or to molecular size (simple versus complex carbohydrate) remains to be established.

Animals↗
PubMed1983

Effect of copper deficiency on metabolism and mortality in rats fed sucrose or starch diets.

Copper deficiency was induced in rats by feeding sucrose or starch diets deficient in copper. Copper-deprived rats fed either diet exhibited decreased plasma ceruloplasmin concentration and increased plasma cholesterol. Glucose homeostasis and utilization was impaired both in vivo and in vitro. Oral glucose tolerance was impaired, insulin binding decreased, and CO2 formation and lipogenesis from [U-14C]glucose were decreased. Feeding sucrose but not starch diets deficient in copper magnified the copper deficiency and resulted in 60% mortality. Although both deficient diets contained the same concentration of copper, the hepatic copper concentration of rats fed sucrose was reduced nearly threefold compared to rats fed starch. Reduced epididymal fat pad, increased liver weight, reduced blood hemoglobin and a marked hypertrophy of the heart with gross deformities as well as histopathologic changes were noted only in those rats fed the copper-deficient sucrose diet. The biochemical lesions induced by deprivation of copper can be suppressed by feeding diets containing starch or can be magnified by high sucrose intake.

Adipose Tissue↗
PubMed1983

Immune complexes, gallium lung scans, and bronchoalveolar lavage in idiopathic interstitial pneumonitis-fibrosis.

We obtained results of lung immune complexes (LIC), circulating immune complexes (CIC), 48-hour gallium lung scans (scans), bronchoalveolar lavage (BAL), and pulmonary function tests in 20 patients with idiopathic interstitial pneumonitis-fibrosis. Sixteen patients had predominantly interstitial (13 cases UIP) and/or intraalveolar (3 cases DIP) cellular disease (group 1). Prior to corticosteroid therapy in group 1, scans were positive in 75 percent, CIC were elevated in 86 percent, LIC were present in 64 percent, and BAL was abnormal in 90 percent. Duration of follow-up after treatment was 3.5 +/- 1.0 year. In group 1 after treatment with corticosteroids in 13 patients and corticosteroids and penicillamine (three patients) and plasmapheresis (one patient), only four patients remain stable or improved. After corticosteroid therapy, elevated CIC returned to normal values despite progressive patient deterioration. In three patients, lung immune complexes were still detected after circulating immune complexes had returned to normal after corticosteroid therapy. In group 2 were four patients with fibrotic disease; scans and CIC were uniformly negative, LIC were weakly present in only one patient, and BAL was abnormal in all. Despite corticosteroid therapy, all have died or deteriorated. These results suggest that positive gallium lung scans, BAL, circulating immune complexes, and to a lesser extent, lung immune complexes are associated with the cellular phase of interstitial pneumonia, but do not reliably identify a corticosteroid-responsive group.

Adult↗
PubMed1983

Effect of copper or insulin in diabetic copper-deficient rats.

The effects of copper and insulin on lipogenesis and glucose tolerance were studied using diabetic, copper-deficient rats. Diabetes was induced by intraperitoneal injection of 50 mg streptozotocin/kg body weight to rats fed a sucrose-copper deficient diet for 7 weeks. Five days later the rats were injected intraperitoneally with [14C]glucose with either saline, insulin, copper, or copper plus insulin. The disappearance of serum [14C]glucose at 30, 60, and 120 min postinjection and the incorporation of [14C]glucose into lipid of epididymal fat 2 hr after administration were determined. The combined effect of copper and insulin significantly decreased peak blood glucose at 30 min and increased the incorporation of [14C]glucose into lipid in the epididymal fat pad when compared to either copper or insulin alone. The enhancement of glucose utilization may be due to a formation of a more stable complex which will increase insulin binding and/or decrease its degradation.

Adipose Tissue↗
PubMed1982

Effect of copper on carbohydrate metabolism in rats.

Rats fed a copper-poor diet were found to have a reduced plasma insulin response to an oral glucose load in comparison with rats fed a copper-supplemented diet. In addition, the increment in plasma glucose above the fasting level at 60 min and at 120 min was significantly higher in rats maintained on the copper-poor diets. In vitro glucose incorporation into diaphragm glycogen and into epididymal fat-pad lipids was stimulated greater than twofold by the addition of 100 micrograms/ml CuCl2 to the incubation medium. In tissues of streptozotocin-diabetic rats, the stimulatory effect of copper on glucose incorporation in vitro was also noted, but was significantly smaller. These results indicate that glucose utilization by peripheral tissues and insulin release may be added to the many vital functions for which copper is essential.

Animals↗
PubMed1979

Gas liquid chromatographic studies of [1-14C] palmitate uptake by the perfused guinea-pig heart.

In addition to the uptake of palmitate by the isolated perfused guinea-pig heart, there was a substantial release of longer chain fatty acids into the perfusate amounting to about 50% of the uptake of palmitate. Both the uptake of palmitate and the release of other fatty acids was diminished in the presence of 95% N2. The specific activity of myocardial palmitate was increased under 95% N2. No significant difference in the distribution of radioactivity between the different myocardial fatty acids occurred between 95% O2 and 95% N2.

Animals↗
PubMed1978

Effect of papain on experimental amyloidosis.

Experimental amyloidosis was induced in mice by repeated injections of complete Freund's adjuvant (CFA) reinforced with a bacterial vaccine. Papain was administered i.p. at various time intervals during the treatment with CFA. Amyloidosis was found only in the spleen and the liver. No statistically significant differences were found between the papain-treated and the control groups. It is assumed that, although papain releaseed the polysaccharide moiety from the polysaccharide protein complex, the released polysaccharides were most probably bound by electrostatic forces to the amyloid fibres, and did not interfere with amyloidogenesis.

Amyloidosis↗