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Biomedical subjects

T N Robinson

Publications and source records attributed to T N Robinson.

At least 55 records · Page 3Linked to original sources
PubMed1996

Ethnicity and body dissatisfaction: are Hispanic and Asian girls at increased risk for eating disorders?

PURPOSE: To compare prevalences and correlates of body dissatisfaction among white, Hispanic, and Asian girls. METHODS: A total of 939 6th and 7th grade girls (mean age 12.4 years) attending four middle schools in northern California completed self-administered assessments of age, ethnicity, desired body shape, parent education levels, mother's and father's body shapes, pubertal stage, and body dissatisfaction. Body dissatisfaction was assessed with the Body Dissatisfaction scale of the Eating Disorder Inventory. Height, weight, triceps skinfold thickness, and waist and hip circumferences were measured by trained examiners. RESULTS: Hispanic girls reported significantly greater body dissatisfaction than white girls, with Asian girls in-between. After adjustment for body mass index (weight/height), normal and overweight white, Hispanic, and Asian girls reported similar levels of body dissatisfaction. However, among the leanest 25% of girls, Hispanics and Asians reported significantly more body dissatisfaction than white girls. Body mass index was the strongest independent predictor of increased body dissatisfaction in all three ethnic groups. Shorter height among white girls and taller height among Asian girls also made significant independent contributions. Parent education level, a measure of socioeconomic status, was not significantly associated with body dissatisfaction. CONCLUSIONS: Body dissatisfaction is not limited to white girls in middle and upper socioeconomic strata. These findings suggest Hispanic and Asian girls may be at greater risk for adopting eating disorder behaviors than previously recognized.

Adolescent↗
PubMed1995

Effects of chronic stress on sleep in rats.

The present study was conducted to determine the effects of chronic stress on sleep using a rodent paradigm of around-the-clock signalled intermittent foot shock in which some rats can pull a chain to avoid/escape shock while another group of rats is yoked to the first group. We measured sleep using telemetry; four-channel EEG was collected 24 h/day in rats during 2 prestress days; days 1, 2, 3, 7, and 14 during chronic stress; and 3 poststress days. States of REM sleep, non-REM (NREM) sleep, and waking were scored for each 15-s period of the EEG recordings. During the prestress period, rats slept (REM plus NREM) 55% of available time during the light hours and 34% of the dark hours with the remainder represented by waking. On the first day of stress, total sleep and, especially REM sleep, decreased markedly. By the second day of stress, only REM sleep in the controllable stress group (but not the uncontrollable stress group) was still significantly decreased compared to prestress levels, and REM sleep returned to baseline levels by day 7 of stress. The recovery of sleep quantity was accomplished by increased sleep during the dark hours, resulting in a long-lasting disruption of normal circadian sleep patterning.

Animals↗
PubMed1994

Timing and rate of sexual maturation and the onset of cigarette and alcohol use among teenage girls.

OBJECTIVE: To test the hypothesis that the patterns of pubertal progression, early vs late puberty and fast vs slow, are associated with the age at which girls start to drink alcohol and smoke cigarettes. DESIGN: The study included 1463 female students, 10.7 to 18.2 years of age, who were assessed five times during the 2.7-year study. Data regarding pubertal stage, alcohol use, and cigarette use were obtained at each assessment. These data were used to calculate two indexes of pubertal development, the age at which the midpoint of puberty was achieved and the rate of progression through puberty, and the ages when each subject first drank, first drank moderate amounts of alcohol, and first smoked. RESULTS: Girls with earlier puberty (midpoint < 12.2 years) first reported drinking any alcohol at a median age of 12.5 years, 0.7 years younger than girls whose puberty was later. Similarly, girls with earlier puberty reported drinking moderate amounts of alcohol at a median age of 13.7 years, 0.9 years younger than girls with later puberty. Girls with earlier puberty further reported first smoking cigarettes at a median age of 12.8 years, 0.6 years younger than girls with later puberty. The rate of pubertal progression was significantly associated only with the age when girls first drank moderate amounts of alcohol. CONCLUSION: Earlier puberty is associated with a younger age of onset for both drinking and smoking among adolescent girls.

Adolescent↗
PubMed1994

Pursuit of thinness and onset of eating disorder symptoms in a community sample of adolescent girls: a three-year prospective analysis.

Community-based prospective studies are needed to shed light on mechanisms that may influence development of eating disorders and identify variables that could serve as potential targets for prevention efforts. In this paper we examine level of weight preoccupation and other variables prospectively associated with age of onset of eating disorder symptoms over a 3-year interval in a community sample (N = 939) of young adolescent girls. 3.6% (32/887) experienced onset of symptoms over the interval. Only one factor, a measure of Weight Concerns, was significantly associated with onset (p < .001). Girls scoring in the highest quartile on the measure of Weight Concerns had the shortest survival time (12% incidence by age 14.5) and those scoring in the lowest quartile had the highest survival time (2% incidence by age 14.5; p < .001). This finding is consistent with both theoretical and clinical perspectives and represents one of the first prospective demonstrations of a linkage between weight and body shape concerns and later onset of eating disorder symptoms. An understanding of the independent variables that predispose girls to development of symptoms is a useful step towards the establishment of a rational basis for the choice of a prevention intervention target.

Adolescent↗
PubMed1993

Defining obesity in children and adolescents: clinical approaches.

For clinical utility, obesity should be defined as a condition of excess adipose tissue associated with adverse health outcomes. Based on a number of criteria, body mass index (BMI) (weight/height) is the most appropriate measure for clinical assessment of adiposity in children and adolescents. However, sufficient information regarding associations between adiposity and current or future morbidity is lacking. Available data suggest a definition of obesity based on adiposity alone would perform poorly as a clinical screening test for adverse health outcomes. In addition, labeling and attempted weight control therapy may produce more harm than benefit. Therefore, until better information regarding the risks of adiposity and risks of treatment are available, recommendations for weight control therapy should be focused primarily on those children and adolescents who currently manifest adiposity-related morbidity, those with a BMI above the 95th percentile, or those above the 85th percentile who perceive their adiposity to be a significant psychosocial problem. To produce a clinically useful definition of obesity, longitudinal data should be used to determine the sensitivities, specificities, and predictive values of comparative measures of childhood and adolescent adiposity for predicting current and future morbidity, and to evaluate the utilities of including characteristics such as age, age of adiposity rebound, persistence of increased adiposity, family adiposity, family morbidities, and fat distribution to improve predictive values and minimize misclassification. Weight control research should attempt to identify patient characteristics that predict long-term treatment success, treatment failure, and treatment side effects.

Adipose Tissue↗
PubMed1993

Does television viewing increase obesity and reduce physical activity? Cross-sectional and longitudinal analyses among adolescent girls.

To examine the relationships between hours of television viewing and adiposity and physical activity among female adolescents, a cohort study with follow-up assessments 7, 14, and 24 months after baseline was conducted. All sixth- and seventh-grade girls (N = 971) attending four northern California middle schools were eligible to participate. Six hundred seventy-one students had sufficient data for baseline cross-sectional analyses, and 279 students in a no-intervention cohort had sufficient data for longitudinal analyses. The baseline sample had a mean age of 12.4 years and was 43% white, 22% Asian, 21% Latino, 6% Pacific Islander, 4% black, 2% American Indian, and 2% other. Hours of after-school television viewing, level of physical activity, and stage of sexual maturation were assessed with self-report instruments. Height, weight, and triceps skinfold thickness were measured and body mass index (ratio of weight [in kilograms] to height [in meters] squared) and triceps skinfold thickness were adjusted by level of sexual maturity for the analyses. Baseline hours of after-school television viewing was not significantly associated with either baseline or longitudinal change in body mass index or triceps skinfold thickness. Baseline hours of after-school television viewing was weakly negatively associated with level of physical activity in cross-sectional analyses but not significantly associated with change in level of physical activity over time. All results were essentially unchanged when adjusted for age, race, parent education, and parent fatness. Among adolescent girls, television viewing time appears to have only weak, if any, meaningful associations with adiposity, physical activity, or change in either over time.

Adolescent↗
PubMed1992

Low self-esteem in differentiating fearful and self-conscious forms of shyness.

Differences between fearfully and self-consciously shy individuals in self-esteem were investigated. Analysis indicated that fearfully (n = 45) compared to self-consciously (n = 40) shy individuals self-reported lower self-esteem. This result suggests that the role of low self-esteem may be different for each shyness subtype. A possible explanation was proffered.

Adolescent↗
PubMed1991

Effects of MK-801 on learning and memory as assessed using a novel water maze.

The effects of the NMDA receptor antagonist MK-801 [(+)-10,11-dihydro-5-methyl-5H-dibenzo [a,d]-cyclohepten-5,10 imine hydrogen maleate] on learning and memory were assessed using a water maze. The maze was a traditional type of maze with alleys and choices between various paths, but set inside a pool of water to a height of 25 cm. Different mazes could be configured by altering the arrangement of open vs. closed doors. Both the time required to reach an out-of-the-water exit platform and the errors made during the swim from start to finish were recorded. Learning was assessed during the first 10 to 20 trials in a new maze configuration, while memory was tested after the maze was well learned. Three experiments, some with several phases, were performed. These experiments compared the effects of 0.1 mg/kg of either (+)-MK-801, or (-)-MK-801 vs. saline on learning new maze configurations as well as swimming well-learned mazes. Neither of the MK-801 isomers impaired performance of a previously learned maze. (+)-MK-801 clearly slowed learning of new mazes as measured by both maze completion time and errors committed, while (-)-MK-801 had a significant but smaller effect on learning. Rats given (+)- or (-)-MK-801 (0.1 mg/kg) for 16 days while learning one maze and then challenged to learn a new maze without drug administration performed no differently on the new maze than controls, suggesting that the acute effect of MK-801 on learning is not long lasting.

Animals↗
PubMed1991

Concordance between anxiety and autonomic nervous system activity in subjects at genetic risk for affective disorder.

Correlations between electrodermal and heart rate indices of autonomic nervous system (ANS) activity and measures of state and trait anxiety were examined in 22 high-risk subjects, who had a parent with bipolar affective disorder, and in controls. Relatively consistent and significant correlations between anxiety and ANS "arousal" at rest and under stress were found in high-risk subjects, but not in controls. Relationships between electrodermal laterality and anxiety, and between electrodermal activity and heart rate, were also observed only in the high-risk group. The data suggest a unique concordance between various manifestations of anxiety in high-risk persons which may effectively increase the salience of stressful events and the sensitization to stress.

Adolescent↗
PubMed1991

A comparison of [3H]MK-801 and N-[1-(2-thienyl)cyclohexyl]-3,4-[3H]piperidine binding to the N-methyl-D-aspartate receptor complex in human brain.

The binding of (+)-[3H]5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-imine maleate ([3H]MK-801) and N-[1-(2-thienyl)cyclohexyl]-3,4-[3H]piperidine ([3H]TCP) to the N-methyl-D-aspartate (NMDA) receptor complex of human brain has been investigated. Significant differences were noted between the binding of the two ligands in the same tissue samples. Binding of both ligands was stimulated by addition of glutamic acid or glycine. However, addition of both compounds resulted in an additional effect with [3H]MK-801 but not [3H]TCP binding. Saturation analysis revealed approximately twice as many high-affinity sites for [3H]MK-801 (Bmax, 1,500 +/- 300 fmol/mg of protein) than for [3H]TCP (Bmax, 660 +/- 170 fmol/mg of protein). In addition, a low-affinity site was detected for [3H]MK-801 binding but not [3H]TCP binding. The pharmacology of the high-affinity [3H]MK-801 and [3H]TCP binding sites was similar with rank order of potency of inhibitors being MK801 greater than TCP greater than phencyclidine greater than N-allylnormetazocine (SKF 10047). 2-Amino-5-phosphonopentanoate inhibited binding of both ligands with comparable potency whereas both 7-chlorokynurenic acid and ZnCl2 were more potent inhibitors of [3H]MK-801 than of [3H]TCP binding. All compounds examined exhibited Hill coefficients of significantly less than unity. Saturation analysis performed in the striatum revealed that the number of binding sites was the same for both [3H]MK-801 (Bmax, 1,403 +/- 394 fmol/mg) and [3H]TCP (Bmax, 1,292 +/- 305 fmol/mg). Addition of glutamate or glycine stimulated striatal binding but there was no further increase on addition of both together.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

The effects of GABAB receptor agonists and antagonists on potassium-stimulated [Ca2+]i in rat brain synaptosomes.

The effects of GABAB agonists and putative antagonists on intrasynaptosomal calcium ion concentrations ([Ca2+]i) after stimulation with potassium ions were studied with the fluorescent probe Quin 2. gamma-Aminobutyric acid and (-)-baclofen, but not (+)-baclofen, produced a dose-dependent inhibition of the potassium-stimulated [Ca2+]i in cortical synaptosomes from the rat. This effect was mimicked by another GABAB agonist SL75102 and weakly by muscimol. It was not inhibited by the alpha-adrenoceptor antagonist phentolamine. This system thus appears to provide a useful test of GABAB receptor function. None of the putative GABAB antagonists, phaclofen, delta-aminovaleric acid or beta-phenyl GABA inhibited responses to (-)-baclofen. Indeed, all three compounds produced similar responses to that seen with (-)-baclofen, suggesting that they act as agonists in this system. These data suggest that those GABAB receptors modulating [Ca2+]i have a distinct pharmacology from post-synaptic GABAB receptors, defined in electrophysiological experiments.

Animals↗
PubMed1989

The mechanism of tetrahydroaminoacridine-evoked release of endogenous 5-hydroxytryptamine and dopamine from rat brain tissue prisms.

1 Tetrahydroaminoacridine (THA) is an acetylcholinesterase (AChE) inhibitor which may have a greater therapeutic effect in Alzheimer-type dementia (ATD) than other cholinergic agents. This suggests possible non-cholinergic properties. We have therefore studied the effects of THA on the release of endogenous 5-hydroxytryptamine (5-HT) from rat cortical prisms and dopamine from striatal prisms. 2 In the presence of K+ (1 mM), THA stimulated release of both 5-HT and dopamine. THA (100 microM)-evoked monoamine release was comparable, but not additive with the release produced by K+ (35 mM). The effect was not maximal at 1 mM THA. THA-evoked release of 5-HT was independent of the presence of Ca2+ in the external medium. 3 Drugs acting on the cholinergic system, nicotine, mecamylamine, atropine, oxotremorine, physostigmine and neostigmine (all 10 microM) had no effect on 5-HT and dopamine-release. 4-Aminopyridine (4-AP), a potent acetylcholine-releasing agent, had no effect on 5-HT release and was approximately 100 fold less active than THA on dopamine release. 4 Both THA and reserpine enhanced the release of 5-HT in the presence of the monoamine oxidase inhibitor, pargyline. Reserpine- but not THA-evoked release was abolished in the absence of pargyline. Reserpine (5 mg kg-1, i.p.) markedly depleted brain monoamine concentrations 3 h after injection, while THA (15 mg kg-1, i.p.) had no effect. 5 Chloroamphetamine and fenfluramine both released 5-HT in a Ca2(+)-independent manner and with a similar potency to THA, while (+)-amphetamine released dopamine with a similar potency to THA. The effects of the amphetamines were not maximal at 1 mM. However, unlike THA, chloroamphetamine-evoked release of 5-HT was additive with release evoked by K+ (35 mM). 6 Clomipramine (IC50 = 0.036 microM) and THA (IC50 = 19.9 microM) all inhibited the uptake of [3H]-5-HT into a P2 membrane preparation. However, none of these compounds inhibited [3H]-5-HT uptake into tissue prisms during the release experiments in which the reuptake inhibitor fluoxetine (5 microM) was present. 7 We conclude that THA does not release endogenous 5-HT through a cholinergic, reserpine- or amphetamine-like mechanism or through inhibition of reuptake. The possibility exists that the release may occur via blockade of 4-AP-insensitive K+ channels.

Aminoacridines↗
PubMed1989

Effects of the putative antagonists phaclofen and delta-aminovaleric acid on GABAB receptor biochemistry.

1. Phaclofen and delta-aminovaleric acid (delta-AVA) have been reported to be antagonists at gamma-aminobutyric acidB (GABAB) receptors. Phaclofen, delta-AVA and related compounds were examined for potency and specificity at GABAB and GABAA receptors in rat cortical membranes labelled with [3H]-(-)-baclofen and [3H]-muscimol, respectively. Additionally phaclofen and delta-AVA were examined in two functional tests of central GABAB activity in rat cortical slices, namely the inhibition of forskolin-stimulated cyclic AMP accumulation, and the potentiation of isoprenaline-stimulated cyclic AMP accumulation. 2. delta-AVA (IC50 = 11.7 microM) was 20 fold more potent than phaclofen (IC50 = 229 microM) on GABAB receptor binding. All compounds possessing a phosphonic acid group, including phaclofen, which were active at GABAB receptors were inactive at GABAA receptors, while delta-AVA was equally potent at both receptors. Several compounds exhibited Hill coefficients of less than unity in displacing [3H]-(-)-baclofen binding. 3. (-)-Baclofen inhibited forskolin-stimulated cyclic AMP accumulation (IC50 = 7.9 microM) but this effect was not stereospecific. Phaclofen (1 mM) was inactive against this inhibition but produced a potentiation of the forskolin effect. delta-AVA (1 mM) failed to antagonize the effect of baclofen; rather it mimicked baclofen. 4. (-)-Baclofen (10 microM) potentiated isoprenaline-stimulated cyclic AMP accumulation, an effect antagonized by phaclofen (1 mM). delta-AVA (1 mM) may be a weak antagonist but also potentiated basal cyclic AMP accumulation. 5. We conclude that neither delta-AVA nor phaclofen are potent specific GABAB receptor antagonists.

Amino Acids↗
PubMed1989

The modulation by chlormethiazole of the GABAA-receptor complex in rat brain.

1. The interactions of chlormethiazole with gamma-aminobutyric acid (GABA) synthesis and release, and with ligand binding to sites associated with the GABAA-receptor complex and the GABAB-receptor have been studied in the rat. The GABAA-receptor was studied using [3H]-muscimol, [3H]-flunitrazepam was used to label the benzodiazepine modulatory site, and [35S]-butyl-bicyclophosphorothionate ([35S]-TBPS) to label the chloride channel. 2. Chlormethiazole had no effect on GABA synthesis in the cortex, hippocampus and striatum or on GABA release from cortical slices in vitro. Chlormethiazole did not displace [3H]-baclofen binding to the GABAB-receptor. 3. Chlormethiazole (IC50 = 140 microM) and pentobarbitone (IC50 = 95 microM) both inhibited [35S]-TBPS binding by increasing the rate of [35S]-TBPS dissociation. In addition, chlormethiazole caused an apparent decrease in the affinity of [35S]-TBPS binding. 4. Chlormethiazole enhanced the binding of [3H]-muscimol but had no effect on [3H]-flunitrazepam binding. In contrast, the sedative barbiturate pentobarbitone enhanced both [3H]-muscimol and [3H]-flunitrazepam binding. 5. It is concluded that the sedative and anticonvulsant effects of chlormethiazole are probably mediated through an action at the GABAA-receptor. However, chlormethiazole does not interact with the GABAA-receptor complex in an identical manner to the sedative barbiturate pentobarbitone.

Animals↗
PubMed1989

The Stanford Adolescent Heart Health Program.

This study was designed to create, implement, and test a school-based multiple risk factor reduction program for high school students. All tenth graders in four senior high schools (N = 1447) from two school districts participated in the study. Within each district, one school was assigned at random to receive a special 20-session CVD risk reduction intervention and one school served as a control. The schools were matched for size and distribution of racial groups before randomization. At a two-month follow-up, knowledge gains were significantly greater for students in the treatment group on each of the risk factor domains tested: nutrition/diet (p less than 0.0001), physical activity (p less than 0.0001), and cigarette smoking (p less than 0.0001). Compared to controls, a higher proportion of those in the treatment group who were not exercising regularly at baseline, reported regular exercise at follow-up (p less than 0.0003). Almost twice as many baseline experimental smokers in the treatment group reported quitting at follow-up while only 5.6% of baseline experimental smokers in the treatment group graduated to regular smoking compared to 10.3% in the control group (p = 0.009). Students in the treatment group were more likely to report that they would choose heart healthy snack items (p less than 0.0001). Beneficial treatment effects were observed for resting heart rate (p less than 0.0001), BMI (p = 0.05), triceps skinfold thickness (p = 0.003), and subscapular skinfold thickness (p = 0.01). The results suggest that it is feasible to provide CVD risk reduction training to a large segment of the population through school-based primary prevention approaches.

Adolescent↗