Biomedical subjects

N Vaisman

Publications and source records attributed to N Vaisman.

At least 37 records · Page 2Linked to original sources

PubMed1994

Changes in body composition, resting energy expenditure, and thermic effect of food in short children on growth hormone therapy.

The effect of growth hormone (GH) treatment on body composition, resting energy expenditure (REE), and the thermic effect of food (TEF) was studied in 10 prepubertal boys (aged 6.2 to 9.5 years, with subnormal spontaneous GH secretion during the first 6 months of treatment [0.2 IU/kg.dl]). Patients were studied before and at 2, 4, and 6 months after commencing treatment. Height and weight increased significantly during treatment (112.2 +/- 4.5 to 117.2 +/- 6.0 cm and 18.0 +/- 2.8 to 20.8 +/- 3.2 kg, respectively). Body fat percent decreased significantly (15.93% +/- 4.08% to 11.97% +/- 3.30%, P < .0002), but was not different at 4 and 6 months. Total body potassium (TBK) increased significantly (39.15 +/- 5.77 to 48.70 +/- 6.35 g, P < .001) during treatment. When correcting for the expected changes in body composition over time, height and weight were still shown to increase, fat percent decreased significantly, but TBK and mid-arm muscle circumference (MAMC) were not different from the expected values. REE increased significantly during treatment, but when it was expressed per TBK or corrected for the change in kilograms of fat-free body mass (FFBM), it increased only at 2 months and stabilized thereafter. The TEF was increased at 2 and 4 months of treatment and returned to pretreatment levels at 6 months of treatment. Substrate utilization as studied by indirect calorimetry pointed toward a significant protein-sparing effect during the first 4 months of treatment; this change tended to disappear in resting energy metabolism by 6 months of GH treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Composition↗

PubMed1994

Increased neutrophil chemiluminescence production in patients with cystic fibrosis.

Increased free radical production has been suggested as a possible mechanism involved in lung deterioration of patients with cystic fibrosis (CF). Vitamins A and E are known to be involved in the defense mechanism preventing damage caused by free radicals. Both vitamins are fat-soluble and are therefore malabsorbed in patients with CF. We hypothesized that low concentrations of vitamins A and E may be involved in the increased free radical production of these patients. Neutrophils' chemiluminescence and superoxide and hydrogen peroxide production were examined in 11 patients with CF aged 4 to 14 years, and 10 age-matched healthy controls. All our patients were on prolonged supplementation with vitamins A and E, but the control group was not supplemented. Serum vitamins A and E levels and neutrophil vitamin E concentrations were examined concomitantly. Chemiluminescence production was increased 10 minutes after neutrophil stimulation by phorbol myristate acetate (PMA) as compared with that in normals (20,400 +/- 9,463 v 11,990 +/- 3,778 cpm, P < .03). No difference was found in superoxide or hydrogen peroxide production between CF patients and controls. Serum vitamin A levels were significantly higher in CF patients compared with healthy controls (0.641 +/- 0.049 v 0.398 +/- 0.038 mg/L, P < .04) and so were vitamin E levels (13.94 +/- 2.25 v 5.64 +/- 1.15 mg/L, P < .05). Neutrophil vitamin E concentrations were higher in CF patients compared with healthy controls (70.8 +/- 26.0 v 23.6 +/- 9.0 micrograms/10(6) cells). We conclude that neutrophils from CF patients exhibit increased chemiluminescence activity not related to increased free radical production or fat-soluble vitamin deficiency.

Adolescent↗

PubMed1994

Malabsorption in infants with congenital heart disease under diuretic treatment.

Intestinal absorption and its relationship to increased total body water was studied in seven infants with congenital heart disease receiving regular diuretics due to congestive heart failure. All infants and six age-matched healthy controls were studied for a 3-d period during which time all food intake was recorded, stools were collected, and total body water content (TBW) and extracellular water were measured. All the anthropometric measurements were lower in the infants with congenital heart disease compared with healthy controls. Energy and fat excretion in the stools were significantly increased in the group of patients, but when expressed as a percentage of daily caloric intake or as a percentage of the specific intake (e.g. fat excretion/fat intake x 100), no statistical differences were found. TBW as a percentage of body weight was increased in our patients compared with our controls (84.95 +/- 5.82% versus 68.65 +/- 4.60%; p = 0.01) and so was extracellular water as a percentage of predicted (200.0 +/- 18.6% versus 100.9 +/- 7.2%; p = 0.001). A positive correlation was found between energy and fat excretion as a percentage of the intake and TBW as a percentage of predicted; energy and fat malabsorption did not exceed 8% in the patients with the highest body water content (120% of predicted). It is concluded that malabsorption is not a significant factor in failure to thrive of patients with congenital heart disease who are receiving regular diuretics. Based on the significant negative correlation between excess body water and fat and calorie absorption, however, it is suggested to monitor TBW in patients who fail to gain weight.

Body Water↗

PubMed1993

Effect of chemotherapy on the energy and protein metabolism of children near the end of treatment for acute lymphoblastic leukemia.

Eight children in the final 3 mo of chemotherapy for acute lymphoblastic leukemia were studied while on oral 6-mercaptopurine (6MP) maintenance therapy and then again 4-9 mo after chemotherapy had been completed. Six of the eight were also studied a second time while on 6MP in the 24-h period after receiving intravenous methotrexate (MTX). 6MP reduced protein oxidation after a test meal and reduced fasting urinary urea excretion by enhancing the reutilization of endogenous amino acids for protein synthesis. MTX had no detectable effects on protein metabolism but reduced overnight carbohydrate utilization by enhancing fat utilization. A similar enhancement of fat utilization was evident after a test meal. The two drugs in combination resulted in effects on protein and energy metabolism that were the sum of the individual effects plus an increase in the rate of whole-body protein turnover and synthesis.

Adolescent↗

PubMed1992

Changes in body composition of patients with subnormal spontaneous secretion of growth hormone, during the first year of treatment with growth hormone.

The effects of 1 year of growth hormone (GH) therapy were studied in 10 subjects with subnormal spontaneous secretion of GH, whose ages ranged from 6.5 to 12.4 years. Height, weight, body fat percentage, total body potassium (TBK), and extracellular water (ECW) were measured prior to initiating the treatment, and thereafter at 6 months (period 1) and 12 months (period 2). Height velocity almost doubled during the year of treatment: 7.8 +/- 0.8 and 7.1 +/- 0.7 cm/yr (P less than .0001) during periods 1 and 2, respectively, as compared with 3.9 +/- 0.6 cm/yr pretreatment. Body fat percentage decreased during period 1 to 18.2% +/- 4.9%, versus 16.3% +/- 4.5% (P less than .02), but stabilized thereafter (16.3% +/- 4.9%). Mid-arm muscle circumference (MAMC) and TBK increased in accordance with the predicted values for age. Body mineral density (BMD) increased both in absolute and standardized terms. No changes were found in ECW during treatment. We concluded that GH treatment in children with subnormal spontaneous secretion of GH has mainly a lipolytic effect on body composition, and that resistance to the lipolytic effect develops during the course of therapy.

Anthropometry↗

PubMed1992

Superoxide production during refeeding in patients with anorexia nervosa.

The effect of undernutrition and refeeding on superoxide production by polymorphonuclear cells (PMN) was studied in 11 girls suffering from anorexia nervosa (AN) and 17 age-matched, normal, healthy, control subjects. Superoxide anion production by PMNs from undernourished AN patients was comparable to normal, while a significant decrease in this function was observed during the initial period of refeeding. After a more extended period of refeeding, superoxide production by PMNs from AN patients increased and gradually returned toward normal values. Superoxide production correlated with length of the refeeding period (RF), weight as a percentage of ideal weight for height (W/H%), and rate of weight gain (WG). These results imply that a variety of physiological parameters, including susceptibility to infection, may be altered by refeeding undernourished patients.

Adolescent↗

PubMed1992

Protein turnover and resting energy expenditure in patients with undernutrition and chronic lung disease.

Whole-body protein metabolism was studied in 11 undernourished cystic fibrosis (CF) patient (7 female), 12 normally nourished CF patients (3 female), 7 anorexia nervosa (AN) patients (all female), and 15 normal control subjects (9 female). Protein turnover was studied by the single dose [15N]glycine method and the cumulative excretion of labeled urinary urea and ammonia. Energy metabolism was studied by open-circuit indirect calorimetry. Contrary to previous reports, no differences were found between the protein turnover of CF groups and the normal control group. However, patients with AN had a negative net protein deposition. Resting energy expenditure was significantly reduced in AN patients and increased in CF patients. The gender of CF patients did not affect protein and energy metabolism but fat mass was higher and fat-free mass was lower in CF females.

Adolescent↗

PubMed1992

Short-chain fatty acid absorption in patients with cystic fibrosis.

Patients with cystic fibrosis (CF) often exhibit malabsorption despite the use of supplemental pancreatic enzymes. Unabsorbed carbohydrates and amino acids can serve as substrates for large intestine anaerobic fermentation, thus increasing excretion of short-chain fatty acids (SCFA) in the feces. Nine patients with CF on regular pancreatic enzyme supplementations in the age range of 5-11 years and one older patient were studied. Three-day stool samples were collected, as were 72-h food records. Stools were analyzed for gross energy, total nitrogen, fat content, and SCFA concentration. A significant difference was found between CF and normal controls in total caloric excretion due to fat malabsorption. No significant difference was found between CF and normal controls in protein or SCFA excretion. Fat excretion as percentage of fat intake was significantly increased in CF patients: 35.3 +/- 10.2% versus 8.0 +/- 3.0%, respectively. These data suggest that carbohydrate supplementation could be more widely used to increase caloric intake in CF patients without causing secondary osmotic diarrhea.

Adolescent↗

PubMed1992

Effect of growth hormone therapy on IGF-I, bone GLA-protein and bone mineral content in short children with and without chronic renal failure.

Chronic renal failure (CRF) in the young is complicated by, among other conditions, growth retardation, hyperparathyroidism and uremic osteodystrophy. Many children with CRF are now being treated with growth hormone (GH). Since GH has a direct mitogenic effect on osteoblasts in culture, we studied the effects of GH therapy on osteoblastic activity, such as serum alkaline phosphatase (AP), bone GLA-protein (BGP) and bone mass density (BMD) in poorly growing children with and without CRF. Fifteen (4 girls, 11 boys) healthy children with short stature (SS) and 10 (3 girls, 7 boys) children with end-stage renal failure (CRF) 4.5-12.4 years of age were treated with daily subcutaneous injections of GH in a dose of 0.1-0.125 IU/kg/day for 1 year. IGF-I, BGP and BMD of the spine were determined before and after the year of treatment. During GH therapy, a similar increase in height velocity and IGF-I were noted in SS and CRF groups: 3.8 +/- 0.77 to 8.38 +/- 1.25 (p < 0.001) vs. 4.0 +/- 0.6 to 7.14 +/- 1.3 cm/year (p < 0.001) and 7.8 +/- 2.6 to 21.8 +/- 7.5 (p < 0.01) vs. 7.9 +/- 1.3 to 21.5 +/- 5.6 nmol/l (p < 0.01), respectively. AP increased from 205 +/- 27 to 274 +/- 50 IU/l (p < 0.01) in the SS group but not in CRF patients (223 +/- 58 pre- 218 +/- 51 IU/l post-GH therapy).(ABSTRACT TRUNCATED AT 250 WORDS)

Body Height↗

PubMed1992

BHK-21-derived cell lines that produce basic fibroblast growth factor, but not parental BHK-21 cells, initiate neuronal differentiation of neural crest progenitors.

We present evidence that basic fibroblast growth factor (bFGF)-producing cells stimulate primary differentiation of neurons from neural crest progenitors. Baby hamster kidney (BHK-21) cells were stably cotransfected with plasmid pSV2/neo, which contains the gene conferring resistance to the neomycin analog G418 and expression vectors containing the human bFGF cDNA. Various clones, which differed in their bFGF production levels, were isolated. Homogeneous neural crest cells were cultured on monolayers of bFGF-producing, BHK-21-derived cell lines. While the parental BHK-21 cells, which do not produce detectable bFGF, had poor neurogenic ability, the various bFGF-producing clones promoted a 1.5- to 4-fold increase in neuronal cell number compared to the parental cells. This increase was correlated with the levels of bFGF produced by the different transfected clones, which ranged between 2.3 and 140 ng/mg protein. In contrast, no stimulation of neuronal differentiation was observed when neural crest cells were grown on monolayers of parental BHK cells transfected with plasmid pSV2/neo alone, or on a parental BHK-derived clone, which secretes high amounts of recombinant vascular endothelial growth factor (VEGF). Furthermore, the neuron-promoting ability of bFGF-producing cells could be mimicked by addition of exogenous bFGF to neural crest cells grown on the parental BHK line. A similar treatment of neural crest cells grown on laminin substrata, instead of BHK cells, resulted in increased survival of non-neuronal cells, but not of neurons (see also Kalcheim, C. 1989, Dev. Biol. 134, 1-10). Taken together, these results suggest that bFGF stimulates neuronal differentiation of neural crest cells by a cell-mediated signalling mechanism.

Animals↗

PubMed1992

[Cytokines in anorexia nervosa--nutritional or neuroimmunal changes?].

Natural cell-mediated cytotoxicity (CMC), spontaneous release of tumor necrosis factor (TNF-alpha) by mononuclear cells in vitro, and PHA-induced interferon (IFN-gamma) production were examined by standard methods in 14 females with anorexia nervosa (AN) and marked weight loss and in 16 normal matched controls. The results were confirmed by neutralization with monoclonal antibodies. In the anorectic patients there was a significant increase in TNF production (16 +/- 5 vs 4 +/- 3 mu/ml), and depressed CMC (4 +/- 2 vs 10 +/- 3 lytic units per 50/10(6) cells) and IFN-gamma production (172.5 +/- 25 vs 367 +/- 34 mu/ml). Following successful refeeding and nutritional rehabilitation, all values returned to normal. Thus there are changes in cytokines and defective natural cytotoxicity in AN, apparently related to undernutrition and not to neuroimmunomodulation. The increased TNF-release may further suppress food intake and enhance tissue catabolism, suggesting that nutritional rehabilitation should be the earliest therapeutic goal in anorexia nervosa.

Anorexia Nervosa↗

PubMed1992

Vitamin A metabolism in plasma of normal and anorectic women.

Plasma retinol and retinyl ester kinetics were determined following an oral bolus of vitamin A in normal women and in women suffering from anorexia nervosa. Circulating levels of vitamin A and alpha-tocopherol were lower in anorectics than in normals with alpha-tocopherol levels close to minimal adequate levels. This suggests the possibility of deficiencies of other dietary factors. Following an oral bolus, plasma retinol increased more in anorectics than in normals, but transport values were not changed. Retinyl ester levels increased sevenfold more in anorectics than normals with a parallel enhancement in transport. Retinyl esters in plasma of normals and anorectics were present mainly in low-density lipoprotein with lesser amounts in very-low-density and high-density lipoprotein, but only minor amounts were found in chylomicrons. These data were used to calculate a relative dose response and indicated that anorectics had higher values than normals. Anorectics appear to have a lower status of vitamins A and E than normals but no defect in vitamin A metabolism was observed.

Administration, Oral↗

PubMed1991

Tumor necrosis factor-alpha and anorexia--cause or effect?

Tumor necrosis factor-alpha (TNF-alpha) is a principal cytokine that may induce weight loss in malignancies and certain chronic infections. Short-term caloric deprivation has been found to facilitate in vitro TNF-alpha production, while increased spontaneous production of TNF-alpha has been found in patients with anorexia nervosa (AN). In the present work, we studied in vitro TNF-alpha production in other types of chronic undernutrition and the changes in TNF-alpha production during the refeeding of patients with AN. Undernutrition was evaluated by calculating fat body mass (FBM) from skinfold measurements and lean body mass (LBM) by total body potassium (TBK) counting. Spontaneous and induced TNF-alpha production by peripheral blood mononuclear cells (PBMC) was studied in six chronically malnourished patients with no intercurrent infections, seven patients with AN, and 16 age-matched normal healthy subjects. Spontaneous TNF-alpha production was in the normal range in the chronically undernourished subjects (4.3 +/- 1.5 v 5.0 +/- 1.9 U/mL), but significantly increased in the seven patients with AN (221 +/- 327 v 5.0 +/- 1.9 U/mL, P less than .0006). During refeeding of patients with AN, TNF-alpha production decreased to the normal range concomitantly with weight gain. We concluded that chronic undernutrition, in general, is not always associated with increased TNF-alpha production and that it still remains to be determined whether TNF-alpha plays a primary role in the pathogenesis of AN.

Adolescent↗

PubMed1991

Nutritional rehabilitation increases resting energy expenditure without affecting protein turnover in patients with cystic fibrosis.

The effect of nutritional rehabilitation on several nutritional parameters was studied in eight malnourished patients with cystic fibrosis during the first year after gastrostomy tube insertion. Body composition was studied by fat skinfold measurements and by total body potassium count, resting energy expenditure (REE) by indirect calorimeter, and protein turnover by a single dose administration of [15N]glycine. Weight gain was accompanied by a significant increase in the various body compartments: weight 41.4 +/- 7.5 to 46.1 +/- 8.4 kg (p less than 0.0002), fat body mass 5.6 +/- 2.8 to 7.7 +/- 3.4 kg (p less than 0.005) and fat-free body mass (FFBM) 35.7 +/- 6.3 to 38.3 +/- 6.9 kg (p less than 0.0003). REE increased significantly per kg of body weight as well as per kg of FFBM. No significant differences were found in protein turnover during refeeding nor in pulmonary function. We conclude that nutritional support restores body composition, but is accompanied by an increase in energy expenditure. This increase could not be attributed to increased protein turnover.

Adolescent↗

PubMed1991

Effect of refeeding on the energy metabolism of adolescent girls who have anorexia nervosa.

The effect of refeeding on resting energy expenditure (REE) and substrate utilization was studied in 18 hospitalized adolescent girls (aged 12.9-19.1 years) suffering from anorexia nervosa. Changes in body composition were monitored weekly and included weight, fat body mass (FBM), lean body mass (LBM) and total body potassium (TBK). REE was studied weekly by open-circuit calorimetry. Weight gain was noted in all patients (38.2 +/- 5.6 to 44.5 +/- 5.3 kg), involving increased FBM and LBM. REE increased per kg of weight (91.6 +/- 15.1 to 101.7 +/- 18.0 kJ kg-1 d-1) and LBM over the first weeks of refeeding (P less than 0.025) and then stabilized. Substrate utilization showed an increase in carbohydrate and protein utilization (P less than 0.001) during the first few weeks of refeeding. We also studied the thermic effect of food (TEF) in 14 of the 18 subjects. Upon admission the subjects had a reduced TEF (36.4 +/- 24.3 kJ 2 h-1) (P less than 0.001). With refeeding TEF rose to a peak or plateau, then decreased to normal levels (61.9 +/- 36.0 kJ 2 h-1) before discharge from hospital. We conclude that the energy metabolism of adolescent girls adapts to semi-starvation by a reduction in both REE and TEF; with refeeding there is reversal of this adaptive function.

Adolescent↗

PubMed1990

Characterization of the receptors for vascular endothelial growth factor.

Vascular endothelial growth factor (vEGF) is a recently discovered mitogen for endothelial cells. It is also a potent angiogenic factor. We have characterized the vEGF receptors of endothelial cells using both binding and cross-linking techniques. Scatchard analysis of equilibrium binding experiments revealed two types of high-affinity binding sites on the cell surfaces of bovine endothelial cells. One of the sites has a dissociation constant of 10(-12) M and is present at a density of 3 x 10(3) receptors/cell. The other has a dissociation constant of 10(-11) M, with 4 x 10(4) receptors/cell. A high molecular weight complex containing 125I-vEGF is formed when 125I-vEGF is cross-linked to bovine endothelial cells. This complex has an apparent molecular mass of 225 kDa. Two other faintly labeled complexes with apparent molecular masses of 170 and 195 kDa also are detected. Reduction in the presence of dithiothreitol causes a substantial increase in the labeling intensity of the 170- and 195-kDa complexes, suggesting that these complexes are derived from the 225-kDa complex by reduction of disulfide bonds. The labeling of the vEGF receptors was inhibited by an excess of unlabeled vEGF but not by high concentrations of several other growth factors. Suramin and protamine, as well as several species of lectins, inhibited the binding. The expression of functional vEGF receptors was inhibited when the cells were preincubated with tunicamycin, indicating that glycosylation of the receptor is important for the expression of functional vEGF receptors. Pretreatment with swainsonine on the other hand, did not prevent formation of functional receptors. However, the mass of the 225-kDa complex is decreased by 20 kDa when 125I-vEGF is cross-linked to swainsonine-treated endothelial cells.

Animals↗

PubMed1990

Body compartment changes in sick children.

Our studies showed that there are important changes in body composition in children in response to dieting and refeeding. Similarly, we showed changes in body composition in response to renal transplantation, which would be expected to restore more normal homeostasis, but in its early phases changes in body composition are complicated by the use of high doses of drugs, notably steroid. Some of the changes in body composition can be predicted from changes in weight but the majority cannot. Relatively simple measurements like the four skinfolds as a means of determining body fat are surprisingly accurate, except in extremely obese subjects. Similarly, the measurements of fat free body mass are useful. However, this measurement does not discriminate changes within fat free body mass in the proportions of body cell mass versus extracellular mass. Similarly, none of these measurements provide any information regarding the composition of body cell mass with regard to its potassium and protein content (as reflected by total body nitrogen). The main drawback with total body nitrogen measurements is the radiation exposure. Thus, we have had to limit the inclusion of total body nitrogen measurements. It has been estimated that two total body nitrogen measurements provide a gonadal dose of radiation roughly equivalent to that experienced by an individual living in a large North American city, that means 30 to 50 mREM per each total body nitrogen measurement. It becomes ethically possible then to carry out nitrogen measurements where it can be argued that their measurement is essential in monitoring the safety and well being of the subject; or alternatively if the subject's life expectancy is limited.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1990

Determination of fructose metabolic pathways in normal and fructose-intolerant children: a 13C NMR study using [U-13C]fructose.

An inborn deficiency in the ability of aldolase B to split fructose 1-phosphate is found in humans with hereditary fructose intolerance (HFI). A stable isotope procedure to elucidate the mechanism of conversion of fructose to glucose in normal children and in HFI children has been developed. A constant infusion of D-[U-13C]fructose was given nasogastrically to control and to HFI children. Hepatic fructose conversion to glucose was estimated by examination of 13C NMR spectra of plasma glucose. The conversion parameters in the control and HFI children were estimated on the basis of doublet/singlet values of the plasma beta-glucose C-1 splitting pattern as a function of the rate of fructose infusion (0.26-0.5 mg/kg per min). Significantly lower values (approximately 3-fold) for fructose conversion to glucose were obtained for the HFI patients as compared to the controls. A quantitative determination of the metabolic pathways of fructose conversion to glucose was derived from 13C NMR measurement of plasma [13C]glucose isotopomer populations. The finding of isotopomer populations of three adjacent 13C atoms at glucose C-4 (13C3-13C4-13C5) suggests that there is a direct pathway from fructose, by-passing fructose-1-phosphate aldolase, to fructose 1,6-bisphosphate. The metabolism of fructose by fructose-1-phosphate aldolase activity accounts for only approximately 50% of the total amount of hepatic fructose conversion to glucose. It is suggested that phosphorylation of fructose 1-phosphate to fructose 1,6-bisphosphate by 1-phosphofructokinase occurs in human liver (and intestine) when fructose is administered nasogastrically; 47% and 27% of the total fructose conversion to glucose in controls and in HFI children, respectively, takes place by way of this pathway. In view of the marked decline by 67% in synthesis of glucose from fructose in HFI subjects found in this study, the extent of [13C]glucose formation from a "trace" amount (approximately 20 mg/kg) of [U-13C]fructose infused into the patient can be used as a safe and noninvasive diagnostic test for inherent faulty fructose metabolism.

Blood Glucose↗