SEARCH · PubMed Health

Results for “Restrictive”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,081 records · Page 60Linked to original sources

PubMed2006

Surge capacity associated with restrictions on nonurgent hospital utilization and expected admissions during an influenza pandemic: lessons from the Toronto severe acute respiratory syndrome outbreak.

BACKGROUND: Current influenza pandemic models predict a surge in influenza-related hospitalizations in affected jurisdictions. One proposed strategy to increase hospital surge capacity is to restrict elective hospitalizations, yet the degree to which this measure would meet the anticipated is unknown. OBJECTIVES: To compare the reduction in hospitalizations resulting from widespread nonurgent hospital admission restrictions during the Toronto severe acute respiratory syndrome (SARS) outbreak with the expected increase in admissions resulting from an influenza pandemic in Toronto. METHODS: The authors compared the expected influenza-related hospitalizations in the first eight weeks of a mild, moderate, or severe pandemic with the actual reduction in the number of hospital admissions in Toronto, Ontario, during the first eight weeks of the SARS-related restrictions. RESULTS: Influenza modeling for Toronto predicts that there will be 4,819, 8,032, or 11,245 influenza-related admissions in the first eight weeks of a mild, moderate, or severe pandemic, respectively. In the first eight weeks of SARS-related hospital admission restrictions, there were 3,654 fewer hospitalizations than expected in Toronto, representing a modest 12% decrease in the overall admission rate (a reduction of 1.40 admissions per 1,000 population). Therefore, influenza-related admissions could exceed the reduction in admissions resulting from restricted hospital utilization by 1,165 to 7,591 patient admissions, depending on pandemic severity, which corresponds to an excess of 0.44 to 2.91 influenza-related admissions per 1,000 population per eight weeks, and an increase of 4% to 25% in the overall number of admissions, when compared with nonpandemic conditions. CONCLUSIONS: Pandemic modeling for Toronto suggests that influenza-related admissions would exceed the reduction in hospitalizations seen during SARS-related nonurgent hospital admission restrictions, even in a mild pandemic. Sufficient surge capacity in a pandemic will likely require the implementation of other measures, including possibly stricter implementation of hospital utilization restrictions.

Bed Occupancy↗

PubMed1989

Increased binding of epidermal growth factor to placental membranes of intrauterine growth restricted fetal rats.

To examine the relationship between nutrient supply and fetal and placental growth, we examined epidermal growth factor (EGF) binding to membranes prepared from placentas of growth-restricted fetal rats. Intrauterine growth retardation was accomplished by unilateral ligation of the uterine artery; fetal rats on the contralateral uterine horn served as controls. Fetal growth restriction was accompanied by decreased placental wt at 19 and 20 day's gestation and significantly decreased placental glycogen content at 20 and 21 days, 30% and 15%, respectively. Placental DNA content and protein/DNA ratios were similar in the growth-restricted and control groups. Specific binding of 125I-EGF was increased in growth-restricted placentas at 19 and 20 days' gestation by 32% and 16%, respectively. 125I-EGF binding at 20-21 days increased linearly with the extent of placental growth restriction. Competitive binding experiments yielded linear Scatchard plots with an increased receptor density in growth-restricted placenta at 19 and 20 days' gestation, 74% and 60%, respectively. Binding affinities for the EGF receptor were similar in the two groups. The increased binding of EGF to membranes prepared from growth-restricted fetal rats may serve to enhance nutrient uptake under conditions of decreased uterine blood flow.

Animals↗

PubMed2000

Molecular mechanisms of cell cycle block by methionine restriction in human prostate cancer cells.

Previous studies have shown that dietary or pharmacological methionine restriction inhibits growth of human prostate cancer cells in vitro or as xenografts in mice. We undertook the present studies to clarify the molecular mechanisms by which methionine restriction inhibits prostate cancer cell growth. We found that PC-3 and DU 145 cells stopped proliferating within six days in growth medium containing homocysteine in place of methionine. In contrast, proliferation of LNCaP cells was only partially inhibited by the absence of methionine. Using flow cytometry, we found that methionine restriction caused PC-3 cells to arrest in all phases of the cell cycle, but predominantly in the G2/M phase, whereas LNCaP cells accumulated exclusively in the G1 phase. Methionine restriction led to accumulation of the cyclin-dependent kinase inhibitors p21 and p27, as determined by Western blot analysis, and inhibited the enzymatic activities of the cyclin-dependent kinases CDK2 and cdc2, as determined by an in vitro kinase assay: However, methionine restriction had little or no effect on CDK2 or cdc2 protein levels. Methionine restriction also induced PC-3 cells to undergo apoptosis, as indicated by the appearance of a typical nucleosomal ladder on gel electrophoresis of genomic DNA. We conclude that methionine restriction has potential as a novel treatment strategy for prostate cancer.

Apoptosis↗

PubMed1991

Effect of restricted feeding on the relationship between hypophysial portal concentrations of growth hormone (GH)-releasing factor and somatostatin, and jugular concentrations of GH in ovariectomized ewes.

These studies characterized the secretion of GH-releasing factor (GRF) and somatostatin (SRIF) into the hypophysial portal circulation in ewes after long term restricted feeding. In addition, we examined the temporal relationship between the concentrations of these two hypothalamic peptides in portal blood and the concentration of GH in jugular blood. Six sheep were fed 1000 g hay/day (normal feeding) and 6 sheep were fed 400-600 g hay/day (restricted feeding). This resulted in a wt loss of 35% in restricted animals compared with 6% in control animals after 20 weeks. Fluctuations in portal levels of GRF indicated a pulsatile pattern of secretion with approximately 60% of pulses coincident with, or immediately preceding, a GH pulse. Similarly, 65% of GH pulses were associated with GRF pulses. Restricted feeding increased (P less than 0.01) mean ( +/- SEM) plasma GH levels (9.8 +/- 1.4 vs. 2.9 +/- 0.6 ng/ml) and mean GH pulse amplitude (7.9 +/- 1.8 vs. 2.8 +/- 0.3 ng/ml) but did not affect mean GH pulse frequency (6.0 +/- 1.1 vs. 5.7 +/- 1.1 pulses/8 h). The level of feeding had no effect on mean portal concentration of GRF (restricted: 5.5 +/- 0.8, normal: 6.6 +/- 1.4 pg/ml), GRF pulse amplitude (14.7 +/- 2.3 vs. 13.5 +/- 0.7 pg/ml), or GRF pulse frequency (5.3 +/- 1.1 vs. 6.7 +/- 0.9 pulses/8 h). Portal concentrations of SRIF in sheep on a restricted diet were half (P less than 0.01) those of sheep fed a normal diet (10.2 +/- 2.3 vs. 19.6 +/- 1.6 pg/ml). Pulses of SRIF were not significantly associated with changes in GH or GRF concentrations. These data indicate a functional role for hypothalamic GRF in initiating GH pulses. Furthermore, the increase in GH secretion in underfed sheep was most probably due to a decrease in the release of SRIF into hypophysial portal blood. Restricted feeding had no affect on GRF secretion, but because of the reduced exposure of the pituitary gland to SRIF, it is possible that responsiveness to GRF is enhanced.

Animals↗

PubMed1991

Evidence that pretranslational and translational defects decrease serum insulin-like growth factor-I concentrations during dietary protein restriction.

Dietary protein restriction causes GH resistance and decreases serum insulin-like growth factor-I (IGF-I) concentrations. To determine whether pretranslational or translational defects are involved in the decline of serum IGF-I concentrations during protein restriction, we measured hepatic IGF-I mRNA abundance together with the serum IGF-I peptide response to exogenous GH after 1 week of protein restriction (5% casein in diet; P5) in hypophysectomized rats. We compared these responses with those of hypophysectomized rats fed a protein-sufficient diet (15% casein in diet; P15) and given exogenous GH. A single injection of rat GH (200 micrograms/100 g BW) produced a comparable IGF-I mRNA increment in both groups (at 6 h, 7.8 +/- 1.1 arbitrary units in P5 vs. 8.2 +/- 1.1 in P15), but failed to raise serum IGF-I normally in the P5 group (at 6 h, 90 +/- 15 ng/ml in P5 vs. 216 +/- 63 in P15; P less than 0.01). The post-GH decline of the 7.5-kilobase (kb) IGF-I mRNA abundance was faster in P5 than in P15 animals. In another experiment in intact rats subjected to protein restriction, injections of pharmacological doses of rat GH (400 micrograms/100 g BW.day) for 1 week restored liver IGF-I mRNA abundance to normal without normalization of serum IGF-I (403 +/- 91 vs. 713 +/- 53 ng/ml; P less than 0.01). Our data suggest that 1) the machinery involved in the transcription of the liver IGF-I gene is intact in protein-restricted rats, because these animals retain the ability to muster normal IGF-I mRNA responses to high doses of exogenous GH; 2) the stability of the 7.5-kb IGF-I mRNA is probably decreased by the protein restriction, as suggested by the faster decline of the 7.5-kb transcript in P5 than in P15 hypophysectomized rats; and 3) the discrepancy between normal liver IGF-I mRNA abundance and low serum and liver IGF-I peptide concentrations suggests that translational stalling of the IGF-I mRNAs or increased serum IGF-I clearance is involved in the low serum IGF-I concentrations during dietary protein restriction.

Animals↗

PubMed1992

Effect of dietary calcium or phosphorus restriction and 1,25-dihydroxyvitamin D administration on rat intestinal 24-hydroxylase.

1,25-Dihydroxyvitamin D-24-hydroxylase (24-hydroxylase) modulates the biological effects of 1,25-dihydroxyvitamin D [1,25-(OH)2D] in tissues. The presence of 24-hydroxylase in intestinal mucosa and the mass of the intestine suggest that the intestine is a major site of catabolism of 1,25-(OH)2D. How intestinal levels of 24-hydroxylase are regulated under various dietary conditions, such as calcium (Ca) or phosphorus (P) restriction, is poorly understood. In a series of trials on weanling and mature rats, the effects of dietary Ca or P restriction were compared with the effects of exogenous 1,25-(OH)2D3 administration on intestinal 24-hydroxylase activity. Exogenous administration of 1,25-(OH)2D3, by single bolus injection or constant infusion, increased intestinal 24-hydroxylase activity significantly. Dietary Ca and P restriction both resulted in increased plasma 1,25-(OH)2D3 concentrations several-fold above control rat values (P less than 0.001) and to levels higher than those achieved by constant infusion of 1.3 ng 1,25-(OH)2D3/h. Dietary Ca restriction increased intestinal 24-hydroxylase 6- to 20-fold above that of rats fed a Ca-replete diet (P less than 0.001). Dietary P restriction had no significant effect on intestinal 24-hydroxylase activity. These data suggest that dietary Ca restriction results in increased plasma levels of 1,25-(OH)2D3, which, in turn, leads to up-regulation of intestinal 24-hydroxylase. Conversely, dietary P restriction prevents 1,25-(OH)2D3-mediated up-regulation of 24-hydroxylase.

Animals↗

PubMed2001

Reduced placental 11beta-hydroxysteroid dehydrogenase type 2 mRNA levels in human pregnancies complicated by intrauterine growth restriction: an analysis of possible mechanisms.

11beta-Hydroxysteroid dehydrogenase type 2 (11beta-HSD2) inactivates cortisol to cortisone. In the placenta 11beta-HSD2 activity is thought to protect the fetus from the deleterious effects of maternal glucocorticoids. Patients with apparent mineralocorticoid excess owing to mutations in the 11beta-HSD2 gene invariably have reduced birth weight, and we have recently shown reduced placental 11beta-HSD2 activity in pregnancies complicated by intrauterine growth restriction. This is reflected in the literature by evidence of hypercortisolemia in the fetal circulation of small babies. In this study we have determined the levels of placental 11beta-HSD2 mRNA expression across normal gestation (n = 86 placentae) and in pregnancies complicated by intrauterine growth restriction (n = 19) and evaluated the underlying mechanism for any aberrant 11beta-HSD2 mRNA expression in intrauterine growth restriction. 11beta-HSD2 mRNA expression increased more than 50-fold across gestation, peaking at term. Placental 11beta-HSD2 mRNA levels were significantly decreased in intrauterine growth restriction pregnancies when compared with gestationally matched, appropriately grown placentae [e.g. at term DeltaCt (11beta-hydroxysteroid dehydrogenase type 2/18S) 12.8 +/- 0.8 (mean +/- SE) vs. 10.2 +/- 0.2, respectively, P < 0.001]. These differences were not attributable to changes in trophoblast mass in intrauterine growth restriction placentae, as assessed by parallel analyses of cytokeratin-8 mRNA expression. No mutations were found in the 11beta-HSD2 gene in the intrauterine growth restriction cohort, and imprinting analysis revealed that the 11beta-HSD2 gene was not imprinted. Although the underlying cause is unknown, 11beta-HSD2 gene expression is reduced in intrauterine growth restriction pregnancies. These data highlight the important role of 11beta-HSD2 in regulating fetal growth, a known factor in determining fetal morbidity but also the subsequent development of cardiovascular disease in adulthood.

11-beta-Hydroxysteroid Dehydrogenases↗

PubMed2001

Individual state driving restrictions for people with epilepsy in the US.

BACKGROUND: States in the United States vary widely in their approaches to restricting driving for patients with epilepsy. Many states have shortened seizure-free restrictions or have adopted flexible regulations that consider individual clinical factors in determining driving privileges. The authors summarized state driving restrictions for patients with seizures, particularly unpublished regulatory practices, and determined the role and liability of physicians in judging driving safety for patients with epilepsy. METHODS: The authors surveyed motor vehicle administration bureaus in the 50 states and the District of Columbia and compared the laws, regulations, and practices restricting driving for people with epilepsy. Key responses from a questionnaire were confirmed by state motor vehicle administrations with phone interviews and by a signed executive summary. RESULTS: Twenty-eight states, including the District of Columbia, have laws requiring patients with epilepsy to be free of seizures for single fixed periods, with a median restriction of six months (range, 3 to 12 months). Twenty-three states have adopted more flexible approaches to restricting driving, such as varying seizure-free restrictions based on individual clinical factors. Many states allow patients to drive after shorter seizure-free periods than stated in their laws. These practices, however, are usually unpublished and not easily accessible. Physicians helped determine when their patients may drive in 13 states and were not legally shielded for their assessments in six of these states. CONCLUSIONS: States vary widely in how they regulate driving for patients with seizures. These varied regulatory approaches present potentially valuable models to determine how driving might be best regulated to protect public and patient safety optimally while permitting patients with controlled seizures to drive.

Accidents, Traffic↗

PubMed2004

A consistent abnormality in the average local smoothness of fetal heart rate in growth-restricted fetuses affected by severe pre-eclampsia.

An abnormality in cardiovascular regulation during the prenatal period has been suggested to be the pathophysiological link between fetal growth restriction and adult hypertension. The purpose of this study was to determine how consistently abnormal the local smoothness of the very-short-term heart rate is in growth-restricted fetuses associated with severe pre-eclamptic pregnancy. Multifractal Hurst analysis on the structure function of heart rate was performed in control fetuses (n =150), in fetuses affected by severe pre-eclampsia and not showing growth restriction (n =66) and in fetuses affected by severe pre-eclampsia and showing growth restriction (n =58). The very-short-term (< or =15 heart beats) generalized Hurst exponents of the order of -5 to 5 in three groups were compared. Each exponent quantifies an average local heart rate smoothness at 15-successive-heart rate sites, which were specified by the magnitude of the heart rate variation within the sites determined by and positively correlated with the order of the exponent. This means that the fetal heart rates within the sites of q > or =2 have a large fetal heart rate (FHR) variation, and those within the sites of q < or =-2 have a small FHR variation. In the fetuses affected by severe pre-eclampsia and not showing growth restriction, only values of the exponents of the order > or =2 were abnormally lower. In the fetuses affected by severe pre-eclampsia and showing growth restriction, the values of the exponents of all orders were abnormally lower. In conclusion, the local smoothness of heart rate is consistently abnormal regardless of the magnitude of heart rate variation within a very-short-term period in growth-restricted fetuses affected by severe pre-eclampsia.

Adult↗

PubMed2005

Risk of infant mortality among twins in relation to placental abruption: contributions of preterm birth and restricted fetal growth.

While preterm birth and restricted fetal growth are strongly associated with infant mortality, the extent to which these associations are modified by placental abruption remains unknown. A retrospective cohort study was carried out to examine the risk of infant mortality among twins in relation to abruption, and explore the independent contributions of preterm birth and restricted fetal growth to these associations. The study was restricted to women who had delivered twins at 22 weeks' gestation or more and fetuses weighing 500 grams or more in the United States (1989-2000). Risks of preterm birth (less than 37 weeks' gestation), fetal growth restriction and infant mortality, in relation to placental abruption, were evaluated. All analyses were adjusted for potential sociodemographic confounding factors. The association between restricted twin fetal growth and abruption was the strongest among the most severely growth-restricted babies (i.e., less than 1 centile), with the strength of association diminishing with increasing birthweight centiles. The risk of preterm birth among pregnancies with and without abruption were 80.1% and 51.9%, respectively (relative risk [RR] 1.5, 95% confidence interval [CI] 1.4-1.6). The risk of small-for-gestational-age (SGA; birthweight of less than the 10th centile for gestational age) among abruption and nonabruption births was 11.7% and 9.2%, respectively (RR 1.3, 95% CI 1.2-1.4). Compared with twins of the appropriate growth delivered at term, the relative risks for infant mortality in the presence of abruption were 9.9 (95% CI 5.4-18.2) for term-SGA, 25.0 (95% CI 22.3-28.1) for preterm-non-SGA, and 36.2 (95% CI 28.4-46.1) for preterm-SGA births. The association between infant mortality and abruption among twins appears largely mediated through preterm birth, and to a lesser extent, through SGA. The association between fetal growth and abruption is strongest among the severely growth-restricted babies, suggesting that the origins of placental abruption may develop in early pregnancy.

Abruptio Placentae↗

PubMed1975

Severe pleural restriction: the maximum static pulmonary recoil pressure as an acid in diagnosis.

Three patients with pleural restriction are presented in detail. One patient had had a right pneumonectomy and died of ventilatory failure due to left-sided restrictive pleurisy. The second patient had neoplastic pleural effusion and inactive tuberculosis. The third patient had systemic lupus erythematosus with bilateral restrictive pleuritis. The physiologic picture was similar in the three cases, with marked decrease of lung volumes, increase of the RV/TLC ratio, absence of airways obstruction, decrease of the Dco and decrease of dynamic lung compliance. In addition, each of these three patients and others with severe pleural restriction had a lower than normal maximum static pulmonary recoil pressure (Pmax). Since in pulmonary restrictive disease, the Pmax was found to be elevated, it was a useful test for distinguishing pulmonary restriction from pleural restriction.

Adenocarcinoma↗

PubMed1988

Restricted pulmonary function in cystic fibrosis.

Some patients with cystic fibrosis have reduced pulmonary volumes, indicating a restrictive pattern of pulmonary disease. We identified ten patients with pulmonary functional evidence of restriction among 158 patients with cystic fibrosis followed at the University of California San Diego Medical Center in 1984 and 1985. We characterized the radiographic, pulmonary functional, and clinical characteristics of these restricted patients compared to matched nonrestricted patients. Pulmonary volumes were measured by three different techniques: plethysmography; nitrogen washout; and radiography. Except for plethysmographic pulmonary volumes, there were no significant differences between the matched restricted and nonrestricted patients. Radiographic pulmonary volume tended to overestimate gas volume measured by the other techniques. Differences among these techniques (thought to represent air-space filling) correlated best with radiographic evidence of air trapping and bronchial markings and not with parenchymal lesions. Serial pulmonary function tests demonstrated changes in pulmonary volume in several patients and a trend toward improvement in pulmonary volume in the restricted patients over time. We conclude that restricted pulmonary function does not necessarily indicate more severe disease in patients with cystic fibrosis and may be reversible in some. The mechanism of restriction may be related more to radiographic evidence of airway disease than to parenchymal abnormalities.

Adult↗

PubMed1991

Can concomitant restriction be detected in adult men with airflow obstruction?

A reduction in lung volume is used to diagnose physiologic restriction in the pulmonary function tests of patients with lung disease. Airflow obstruction is commonly associated with hyperinflation of static lung volume. Because restriction and obstruction exert opposite effects on lung volumes, we questioned whether the lack of hyperinflation of static lung volumes could indicate the presence of concomitant restriction in patients with airflow obstructive ventilatory defects. To assess this, we evaluated by pulmonary function tests and chest roentgenograms of 58 patients with airflow obstruction (group 1), 18 of whom then sustained various types of resection for lung cancer (group 2) as a type of superimposed restriction. We selected 80 percent of predicted as the lower limit of "normal" frequently used by clinical pulmonary function laboratories. Despite a statistically significant decrease in total lung capacity (p less than 0.05) for the postpneumonectomy patients, when the static lung volume measurements of the patients with resection were evaluated, no one lung volume showed a consistent reduction sufficient to detect the superimposed restriction in all these patients. Using 80 percent of predicted as "normal," 61 percent of our patients with airflow obstruction and superimposed restriction would have been missed. We conclude that it is clinically difficult, based on only static lung volume measurements alone, to detect restriction superimposed on the hyperinflation of airflow obstruction unless these lung volumes are reduced to below accepted "normal" limits.

Aged↗

PubMed2005

Caloric restriction inhibits steroid-induced gonadotropin surges in ovariectomized rhesus monkeys.

We recently reported that caloric restriction inhibited ovulation in rhesus monkeys. The objective of the current study was to determine if caloric restriction affected the positive feedback response to ovarian steroids in non-human primates. Studies were conducted in four long-term ovariectomized rhesus monkeys. Animals were given an estrogen/progesterone challenge while maintained on a normal diet and on a diet that reduced body weight by approx 20%. In all cases, animals were maintained at the desired weight [based on a calculation of body mass index (BMI)] for a minimum of 4 wk before initiating the steroid challenge. Caloric restriction reduced BMI from 23.3 +/- 0.3 to 18.9 +/- 0.2 kg/m2. The estrogen/progesterone challenge elicited an LH and FSH surge in each animal maintained at a normal BMI. By contrast, gonadotropin surges were significantly compromised when monkeys were challenged at a low BMI. In addition to affecting the reproductive axis, caloric restriction stimulated cortisol release and suppressed T3 secretion. These endocrine effects of caloric restriction are consistent with our findings in ovary-intact monkeys. In summary, our previous reports in ovary-intact animals confirmed an effect of caloric restriction on tonic gonadotropin secretion leading to anovulation. Our current results suggest the effects of caloric restriction on the reproductive axis extend beyond inhibition of tonic gonadotropin secretion to include a disturbance of phasic gonadotropin secretion.

Amenorrhea↗

PubMed1998

Insulin unexpectedly increases the glucose 6-phosphate Ka of skeletal muscle glycogen synthase in calorie-restricted monkeys.

In skeletal muscle of normal subjects, the concentration of glucose 6-phosphate (G6P) at which the activity of glycogen synthase (GS) is half maximal (Ka) is decreased by in vivo insulin, and the fractional activity is increased without a change in GS maximal activity (Vmax). We have shown that moderate chronic calorie restriction, previously shown in rodents to be effective in slowing aging, resulted in the prevention of obesity and type 2 diabetes in primates (rhesus monkeys, Macaca mulatta). However, unexpectedly, in a subgroup of calorie-restricted monkeys, insulin during a euglycemic hyperinsulinemic clamp caused an unanticipated decrease in skeletal muscle GS fractional activity. These same monkeys had the lowest whole-body glucose disposal rate (M), the greatest increase in skeletal muscle G6P content and the greatest increase in skeletal muscle glycogen phosphorylase activity during the euglycemic hyperinsulinemic clamp compared to the remaining calorie-restricted monkeys with normal insulin action. To determine whether this highly unusual insulin-mediated decrease in GS fractional activity was due to increased phosphorylation (increased Ka), we measured the activity of skeletal muscle GS at 9 different G6P concentrations before and during the euglycemic hyperinsulinemic clamp in 6 calorie-restricted monkeys. G6P Ka increased (n = 4) and Vmax decreased (n = 5) during the clamp. Basal G6P Ka was inversely related to basal GSfv (r = -0.94, p < 0.002). G6P Ka and skeletal muscle G6P content were positively related under insulin-stimulated conditions (r = 0.93, p < 0.005). The change in G6P Ka (insulin-stimulated minus basal) was inversely related to M (r = -0.94, p < 0.002) and positively related to the change in skeletal muscle G6P content (r = 0.93, p < 0.005). We conclude that moderate calorie restriction results in a reversal of normal insulin action at the skeletal muscle with inactivation of glycogen synthase which is likely to be due to an increase in phosphorylation of GS together with a decrease in Vmax of GS during a euglycemic hyperinsulinemic clamp in most of the calorie-restricted monkeys. These alterations are likely to be involved in the anti-diabetogenic effects of calorie restriction.

Animals↗

PubMedDate not supplied

Caloric restriction for 24 hours increases mean night growth hormone.

UNLABELLED: In obesity, serum growth hormone (GH) is usually low, confounding GH assessment of short obese children. We evaluated whether 24-h caloric restriction would permit better discrimination between normal GH secretion and GH deficiency (GHD) by elevating night GH levels. DESIGN AND PATIENTS: Serum was obtained every 20 minutes 2000-0800 h before and 2200-0400 h after 24 hours of caloric restriction (8% of usual calories) in 24 normal height children [14 normal (weight for height 10-90th percentile); 10 obese (weight for height > 95th percentile)] and in 31 short children (height shorter than -2.0 SD below mean for age). All samples from both nights per child were assayed for GH simultaneously to eliminate interassay variability. RESULTS: Mean GH increased significantly in all groups after caloric restriction (P < 0.01). Obese children had lower baseline mean GH and GH amplitude compared to normal (P < 0.01); GH increased into normal range after restriction. Basal GH studies in short children were not significantly below normal. Surprisingly, some with low stimulated GH increased their night GH into the normal range after caloric restriction. CONCLUSIONS: Caloric restriction for 24 h enhances night GH similarly in short and in normal children, and thus does not increase the diagnostic utility of night GH studies in non-obese short children. Caloric restriction reverses suppressed GH secretory state of obese children, perhaps by decreasing diet-dependent somatostatin inhibition of GH secretion.

Adolescent↗

PubMed2002

Effect of children on home smoking restriction by inner-city smokers.

OBJECTIVE: The home is the site of the most significant environmental tobacco smoke (ETS) exposure for children. Surveys show that adults, including smokers, agree that smoking should be restricted in homes of smokers with children. However, in a national survey, only 12.5% of such homes are actually smoke-free. This study examined factors associated with home smoking restriction among inner-city smokers. METHODS: A cross-sectional survey of 598 adult smokers who attended an inner-city community health center was conducted. RESULTS: Home smoking restriction was reported by 38.2% of all smokers (95% confidence interval [CI]: 33.6%-42.8%). Univariate analysis showed smoking restriction was positively associated with presence of children and of a nonsmoking adult partner in the home, intentional limiting of smoking, stages of change, and fewer number of cigarettes smoked daily. On multivariate analysis, home smoking restriction was more likely with the presence of a child (odds ratio: 2.63; 95% CI: 1.70-4.08) and a nonsmoking adult partner (odds ratio: 2.30; 95% CI: 1.32-4.02) in the home. CONCLUSIONS: The presence of children and of nonsmoking adults is associated with the practice of smoking restriction in the homes of inner-city smokers. These findings suggest that inner-city smokers are concerned about health effects of ETS on children. Health professionals should target nonsmoking adult members of households with children and smokers but no home smoking restriction and emphasize the health effects of ETS on children as a motivation for smoking parents to limit exposure and to quit smoking.

Adult↗

PubMed2003

Extrauterine growth restriction remains a serious problem in prematurely born neonates.

BACKGROUND: Poor growth is a common problem in premature neonates and may be associated with neurodevelopmental delay. OBJECTIVE: To evaluate the incidence of extrauterine growth restriction (growth values < or =10th percentile of intrauterine growth expectation based on estimated postmenstrual age in premature (23-34 weeks' estimated gestational age) neonates at the time they are discharged from the hospital. DESIGN/METHODS: Using a database formed from a computer-assisted tool that generates clinical progress notes and discharge summaries on neonatal intensive care unit admissions, we reviewed data on neonates discharged from 124 neonatal intensive care units between January 1, 1997, and December 31, 2000. We evaluated neonates who were born between 23 and 34 weeks' estimated gestational age without congenital anomalies and who were cared for at and discharged from the same hospital. For each patient, we compared the discharge growth values to the expected values based on our intrauterine growth data and postmenstrual age on the day of discharge. We defined extrauterine growth restriction as having a measured growth value (weight, length or head circumference) that was < or =10th percentile of the predicted value. In each specific birth weight and estimated gestational age group, we counted the number of neonates < or =10th percentile for each growth parameter and calculated the percentage of patients who had values < or =10th percentile at discharge. Using logistic regression, we evaluated the factors associated with extrauterine growth restriction for weight, length, and head circumference. RESULTS: Our sample included 24 371 premature neonates. Data on discharge weight, length, and head circumference was available on 23 970, 17 203, and 20 885 neonates, respectively. The incidence of extrauterine growth restriction was common (28%, 34%, and 16% for weight, length, and head circumference, respectively). For each growth parameter, the incidence of extrauterine growth restriction increased with decreasing estimated gestational age and birth weight. Factors independently associated with extrauterine growth restriction were male gender, need for assisted ventilation on day 1 of life, a history of necrotizing enterocolitis, need for respiratory support at 28 days of age, and exposure to steroids during the hospital course. CONCLUSIONS: Extrauterine growth restriction remains a serious problem in premature neonates especially for neonates who are small, immature, and critically ill.

Apgar Score↗