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Biomedical subjects

S Golden

Publications and source records attributed to S Golden.

At least 37 records · Page 2Linked to original sources
PubMed1981

An empirical investigation of psychotherapy with schizophrenic patients.

We examined the experience of schizophrenic patients who had been in psychotherapy for 1 year or longer. Therapists and their patients in a university-affiliated community mental health center were interviewed. One year later, followup interviews were conducted. Characteristics of participating patients, descriptions of therapy, behavioral changes, and relationships among these variables are reported. A comparison group of schizophrenics not in psychotherapy was interviewed once. The schizophrenic patients who maintain psychotherapies are isolated and quite impaired. Most patients and therapists report that psychotherapy helps; but there is little evidence of improved social functioning. Therapies that are associated with improved patient behavior are often conducted by more experienced therapists, and participants describe the therapeutic relationship in similar terms. Therapies without associated improvement are described in dissimilar terms by the participants. Results support the thesis that the process of psychotherapy with schizophrenics is related to outcome. Implications for training residents are discussed.

Adult↗
PubMed1981

Metabolism of tritium- and 14C-labeled alanine in rats.

[3-3H]- and [U-14C]alanine were administered to starved rats by bolus injection and by continuous infusion. The specific activities of alanine, glucose, and lactate in blood were followed. The tracer kinetics of alanine depended on the site of tracer administration and sampling. Tracer was either administered into the aorta and blood sampled from the vena cava (A-VC mode) or tracer was administered into the vena cava and arterial blood sampled (V-A mode) (Katz, J. F. Okajima, and A. Dunn. Biochem J. 194: 513-524, 1981). When tracer was infused in the A-VC mode the plateau specific activity of alanine was about half that obtained in the V-A mode. The parameters of alanine turnover were calculated from the specific activities obtained in the A-VC mode. The calculated apparent replacement rate averaged 1.9 mg.min-1.kg-1 for [U-14C]- and 3.9 mg.min-1.kg-1 for [3-3H]alanine, indicating a carbon recycling of about 50%. The apparent contribution of alanine carbon to that of glucose is 15%. The maximal activity in plasma water is attained at about 5 min after bolus injection of [3-3H]alanine and that of [14C]glucose in blood is attained about 10 min after the injection of [U-14C]alanine. Maximal specific activity of [3H]- and [14C]lactate is attained within about 1 min after injection. The apparent mean transit time and alanine mass were calculated from the areas of washout curves after the continuous infusion was terminated. The mean transit time for [3H]alanine was 10 min and apparent total body mass of alanine of the order of 40 mg/kg. The apparent means transit time for [U-14C]alanine ranged from 33 to 66 min corresponding to a mass of the order of 100 mg/kg of alanine or 40 mg/kg of alanine carbon.

Alanine↗
PubMed1980

The determination of reduced nicotinamide-adenine dinucleotide and metabolic intermediates in picomole amounts with bacterial luciferase.

Methods that use bacterial luciferase for the assay of NADH in the range from 1 pmol to 1 nmol are described. Optimal conditions for the assay of glycolytic intermediates, tricarboxylic acid-cycle intermediates and related amino acids from milligram amounts of tissue are presented. The whole spectrum of these intermediates can be determined on about 10 mg of liver tissue. The methods are simple, are suitable for routine use, and the instrumentation is inexpensive. The concentrations of glycolytic intermediates in rat livers were determined by conventional spectrometric methods and with luciferase, and the results found to be in good agreement.

Animals↗
PubMed1979

Glycogen synthesis by hepatocytes from diabetic rats.

Hepatocytes prepared from streptozotocin- and alloxan-diabetic rats starved for 24 h contain 0.5--2% wet wt. of glycogen. Glycogen synthesis in the hepatocytes from such rats, after prior depletion of the glycogen by glucagon injection, was studied. As distinct from cells from normal animals, there was no glycogen synthesis from glucose as sole substrate, even at concentrations of 60 mM. When supplied with glucose, a gluconeogenic precursor (lactate, dihydroxyacetone or fructose), and with glutamine there was concurrent synthesis of glucose and of glycogen. Without glutamine there was little or no glycogen synthesis. The rate of glycogen formation was in the same range as for cells from control rats. Glutamine addition markedly activated glycogen synthase in cells of starved diabetic rats, but there was no effect on phosphorylase. We obtained very little synthesis of glycogen with hepatocytes from fed diabetic rats, whereas with normal animals, synthesis by such cells equals or exceeds that obtained from starved rats. The conversion of synthase b (inactive) into the active form was studied in rat liver homogenates. The activation of the synthase in cells from starved diabetic rats is somewhat less than that from normal animals, but that from fed diabetic rats is markedly decreased compared with that in livers of fed control animals or that of starved diabetic animals.

Alloxan↗
PubMed1979

Glycogen synthesis by rat hepatocytes.

1. Hepatocytes from starved rats or fed rats whose glycogen content was previously depleted by phlorrhizin or by glucagon injections, form glycogen at rapid rates when incubated with 10mM-glucose, gluconeogenic precursors (lactate, glycerol, fructose etc.) and glutamine. There is a net synthesis of glucose and glycogen. 14C from all three types of substrate is incorporated into glycogen, but the incorporation from glucose represents exchange of carbon atoms, rather than net incorporation. 14C incorporation does not serve to measure net glycogen synthesis from any one substrate. 2. With glucose as sole substrate net glucose uptake and glycogen deposition commences at concentrations of about 12--15mM. Glycogen synthesis increases with glucose concentrations attaining maximal values at 50--60mM, when it is similar to that obtained in the presence of 10mM glucose and lactate plus glutamine. 3. The activities of the active (a) and total (a+b) forms of glycogen synthase and phosphorylase were monitored concomitant with glycogen synthesis. Total synthase was not constant during a 1 h incubation period. Total and active synthase activity increased in parallel with glycogen synthesis. 4. Glycogen phosphorylase was assayed in two directions, by conversion of glycose 1-phosphate into glycogen and by the phosphorylation of glycogen. Total phosphorylase was assyed in the presence of AMP or after conversion into the phosphorylated form by phosphorylase kinase. Results obtained by the various methods were compared. Although the rates measured by the procedures differ, the pattern of change during incubation was much the same. Total phosphorylase was not constant. 5. The amounts of active and total phosphorylase were highest in the washed cell pellet. Incubation in an oxygenated medium, with or without substrates, caused a prompt and pronounced decline in the assayed amounts of active and total enzyme. There was no correlation between phosphorylase activity and glycogen synthesis from gluconeogenic substrates. With fructose, active and total phosphorylase activities increased during glycogen syntheses. 6. In glycogen synthesis from glucose as sole substrate there was a decline in phosphorylase activities with increased glucose concentration and increased rates of glycogen deposition. The decrease was marked in cells from fed rats. 7. To determine whether phosphorolysis and glycogen synthesis occur concurrently, glycogen was prelabelled with [2-3H,1-14C]-galactose. During subsequent glycogen deposition there was no loss of activity from glycogen in spite of high amounts of assayable active phosphorylase.

Animals↗
PubMed1977

Lipogenesis by hepatocytes of rats with hypothalamic obesity.

Hepatocytes were prepared from livers of rats with bilateral lesions of the ventromedial hypothalamic nucleus (VMN lesioned) and sham-operated control rats. The incorporation of tritium labeled water and 14C glucose and lactate into lipids was studied. Endogenous tritium incorporation into fatty acids in controls ranged from 7-20 muatoms 3H per 100 mg liver protein per hour, and in cells from VMN lesioned rats 25 to 80 muatoms per 100 mg/hour. In both types of cells addition of glucose had no effect on tritium incorporation, but the addition of lactate, pyruvate or alanine stimulated it 30-60%. There was little difference in the labeling of glycerol by the two groups. In cells from fasted refed control or lesioned rats, tritium incorporation was greatly increased and was equal in both groups. Incorporation of glucose carbon in VMN lesioned rats was three to ten times that of controls, but the contribution of glucose carbon to fatty acid synthesis was small.

Animals↗
PubMed1976

Stimulation of hepatic glycogen synthesis by amino acids.

Hepatocytes isolated from livers of fasted rats form little glycogen from glucose or lactate at concentrations below 20 mM. Glycogen is formed in substantial quantities at a glucose concentration of 60 mM. In the presence of 10 mM glucose, 20-30% as much glycogen as glucose is formed from fructose, sorbitol, or dihydroxyacetone. The addition of either glutamine, alanine, or asparagine stimulates the formation of glycogen from lactate 10- to 40-fold. The formation of glucose and glycogen is then about equal, and glycogen deposition in hepatocytes is similar to rates attained in vivo after fasted rats are refed. The amino acids stimulate 1.5- to 2-fold glycogen synthesis from fructose, and 2- to 4-fold synthesis from dihyDROXYACETONE. Ammonium chloride is about one-half as effective as amino acids in stimulating glycogen synthesis when glucose with lactate are substrates. It increased glycogen synthesis 25-50% from fructose but inhibited synthesis from dihydroxyacetone plus glucose.

Alanine↗
PubMed1976

Estimation of glucose turnover and recycling in rabbits using various [3H, 14C]glucose labels.

The glucose replacement rate, percent carbon recycling, mean glucose transit time, and the glucose mass were determined in fasted unanesthetized rabbits after administration of [2-3H,U-14C]-, [3-3H,U-14C]-, [5-3H,U-14C]- or [6-3H,U-14C]glucose using the procedures of Katz et al. (10). The glucose replacement rates and carbon recycling determined with [2-3H,U-14C] and [5-3H,U-14C]glucose are equivalent and greater than those obtained with [3-3H,U-14C]- and [6-3H,U-14C]glucose. Although the means of the glucose replacement rates and percent carbon recycling obtained using [3-3H,U-14C]- and [6-3H,U-14C]glucose are similar, greater variation resulted using the former tracer. Comparisons of detritiation rates and percent carbon recycling using [2-3H,U-14C]- and [6-3H,U-14C]glucose suggest that about 10% of tritium is lost from carbon 2 via futile cycling at the glucose 6-phosphate level. Similarly, comparisons of [5-3H,U-14C]- and [6-3H,U-14C]glucose metabolism suggest that about 10% of tritium lost from carbon 5 occurs via futile cycling at the fructose diphosphate level and/or via the transaldolase reaction. Our results indicate that [6-3H,U-14C]glucose is the more suitable tracer for determining the glucose replacement rate and carbon recycling in vivo.

Animals↗
PubMed1976

Estimation of glucose turnover in rats in vivo with tritium labeled glucoses.

Starved and starved-refed rats were injected intravenously with labelled glucose (a mixture of [2-3H]-, [3-3H]- and [U-14C]glucose with either [5-3H]- or [6-3H]glucose), and the decay of the specific activity of [14C]glucose followed. Glucose was degraded to obtain the 3H/14C ratios for 3 isotope combinations in the same sample. The apparent rates of replacements, apparent carbon recycling, and the body glucose mass were calculated for the different tracers. The 3H/14C ratio from [2-3H, -U-14C]glucose declined much faster than that of the other tracers. Apparent recycling as calculated in fasted rats was 28% for [2-3H, U-14C]- 18% for [5-3H,-U-14C]- 17% for [3-3H, U-14C]- and 14% for [6-3H,U-14C]glucoses. The values in fed rats showed a similar pattern. We estimate that in fasted rats 85 to 90% of the 3HOH liberated from injected [2-3H]glucose is formed by catabolism in the periphery and the rest by recycling in the liver between glucose and glucose 6-P. Detritiation of other labels by hepatic recycling accounts for a very small fraction of the total 3HOH yield.

Animals↗
PubMed1975

Recycling of glucose by rat hepatocytes.

1. The metabolism of glucose labeled uniformly with 14C, and in positions 2, 3 and 5 with tritium by hepatocytes from fed and fasted rats were studied. Cells were incubated with glucose as sole substrate, or with glucose and a variety of glucose precursors, and uptake or production of glucose, and the utilization of the isotopes was determined. 2. There was no uptake of glucose at concentration of up to 15 mM, and net glucose synthesis in the presence of precursors. 14C was however recovered in CO2, lactate and amino acids, and tritium in water. Considerable incorporation into glycogen from 14C and 3H-labeled glucose occurred at high (above 20 mM) glucose concentrations. 3. The yield in water always exceeded that in 14C-labeled products. The yield in 3HOH from [2-3H] glucose exceeded that from [5-3H] glucose, and the latter was greater than from [3-3H] glucose. 4. Utilization of labeled glucose does not follow Michaelis-Menten kinetics. The fractional rate of uptake of 14C and tritium-labeled glucose increases with glucose concentration with a maximum at about 15 mM and then declines. 5. The effect of numerous gluconeogenic substrates on the isotope utilization and the 3H/14C ratio in glycogen was studied. The uptake of 14C was always depressed. Addition of lactate and dihydroxyacetone has little effect on the detritiation of [2-3H] glucose, but it is depressed by other substrates. The detritiation of [3-3H]-and[5-3H]glucose is depressed in gluconeogenesis, that from [3-3H]glucose usually more than from [5-3H]glucose. In the presence of lactate detritiation of [3-3H]glucose is about half that from [5-3H]glucose. 6. Equations to calculate the phosphorylation of glucose and fructose 6-phosphate in the presence of futile cycling between glucose and glucose 6-phosphate and fructose 6-phosphate and fructose 1,6-bisphosphate were derived. 7. The estimate of glucose phosphorylation requires determination of the specific activity of glucose 6-phosphate from [2-3H]glucose. It appears that futile cycling between glucose and glucose 6-phosphate is extensive in cells with a high glycogen content, but is low in cells from starved rats and nearly absent in those from diabetic animals. 8. The estimation of the phosphorylation of fructose 6-phosphate in the presence of cycling requires knowledge of the specific activities of fructose 6-phosphate and fructose 1,6-bisphosphate from [3-3H]glucose. At present there are no adqquate data to calculate phosphorylation and recycling of fructose 6-phosphate, but under some conditions the rate may be quite high.

Amino Acids↗
PubMed1975

Cancer chemotherapy and management of patient problems.

Cancer chemotherapy has made major progress over the past twenty-five years with the development of effective drugs and the application of multiple drug regimens to the treatment of cancer patients. The focus of cancer therapy today is on the cure of cancer with the introduction of multiple modality therapy incorporating surgery, radiotherapy, chemotherapy, and immunotherapy in the treatment of early disease. Thus chemotherapy is becoming commonplace and standard practice, and an awareness of the practical management of drug therapy is essential.

Antineoplastic Agents↗
PubMed1974

Determination of synthesis, recycling and body mass of glucose in rats and rabbits in vivo 3H-and 14C-labelled glucose.

1. Glucose labelled with (3)H in position 2 and uniformly with (14)C was administered simultaneously to rabbits and rats either as a single injection or by continuous infusion. Plasma glucose specific radioactivity and the yield of (3)H in the plasma water were monitored. 2. The rates of synthesis, recycling of carbon and total body mass of glucose were calculated, without assuming a multicompartmental model and without fitting data by exponential expressions. 3. The rate of synthesis of glucose in starved-overnight rabbits was 4mg/min per kg (range 3-4.5mg/min per kg) and 25-35% of the glucose carbon was recycled. The mass of total body glucose in starved rabbits was 290mg/kg (range 220-390mg/kg). About one-third of the total body glucose equilibrates nearly instantaneously with plasma glucose. 4. In rats starved overnight, glucose synthesis was about 10mg/min per kg and recycling of carbon ranged from 30-40%. Total body mass (per kg body weight) is similar to that in rabbits. 5. The activity in plasma water after injection of [2-(3)H]glucose was determined. The initial rate of (3)H(2)O formation is rapid, indicating that the major site of glucose catabolism is in the rapidly mixing pool. The curve of total body glucose radioactivity was obtained from the (3)H(2)O yield, and total mass of glucose was calculated. This agrees with that obtained from the (3)H specific-radioactivity curve.

Animals↗