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Biomedical subjects

K J Campbell

Publications and source records attributed to K J Campbell.

15 recordsLinked to original sources

Family food environment and dietary behaviors likely to promote fatness in 5-6 year-old children.

BACKGROUND: The family food environment (FFE) is likely to exert important influences on young children's eating. Examination of multiple aspects of the FFE may provide useful insights regarding which of these might most effectively be targeted to prevent childhood obesity. OBJECTIVE: To assess the associations between the FFE and a range of obesity-promoting dietary behaviors in 5-6-year-old children. DESIGN: Cross-sectional study. SUBJECTS: Five hundred and sixty families sampled from three socio-economically distinct areas. MEASUREMENTS: Predictors included parental perceptions of their child's diet, food availability, child feeding practices, parental modeling of eating and food preparation and television (TV) exposure. Dietary outcomes included energy intake, vegetable, sweet snack, savory snack and high-energy (non-dairy) fluid consumption. RESULTS: Multiple linear regression analyses, adjusted for all other predictor variables and maternal education, showed that several aspects of the FFE were associated with dietary outcomes likely to promote fatness in 5-6-year-old children. For example, increased TV viewing time was associated with increased index of energy intake, increased sweet snack and high-energy drink consumption, and deceased vegetable intake. In addition, parent's increased confidence in the adequacy of their child's diet was associated with increased consumption of sweet and savory snacks and decreased vegetable consumption. CONCLUSION: This study substantially extends previous research in the area, providing important insights with which to guide family-based obesity prevention strategies.

Beverages↗

Interventions for preventing obesity in children.

BACKGROUND: Obesity prevention is an international public health priority. The prevalence of obesity and overweight is increasing in child populations throughout the world, impacting on short and long-term health. Obesity prevention strategies for children can change behaviour but efficacy in terms of preventing obesity remains poorly understood. OBJECTIVES: To assess the effectiveness of interventions designed to prevent obesity in childhood through diet, physical activity and/or lifestyle and social support. SEARCH STRATEGY: MEDLINE, PsycINFO, EMBASE, CINAHL and CENTRAL were searched from 1990 to February 2005. Non-English language papers were included and experts contacted. SELECTION CRITERIA: Randomised controlled trials and controlled clinical trials with minimum duration twelve weeks. DATA COLLECTION AND ANALYSIS: Two reviewers independently extracted data and assessed study quality. MAIN RESULTS: Twenty-two studies were included; ten long-term (at least 12 months) and twelve short-term (12 weeks to 12 months). Nineteen were school/preschool-based interventions, one was a community-based intervention targeting low-income families, and two were family-based interventions targeting non-obese children of obese or overweight parents. Six of the ten long-term studies combined dietary education and physical activity interventions; five resulted in no difference in overweight status between groups and one resulted in improvements for girls receiving the intervention, but not boys. Two studies focused on physical activity alone. Of these, a multi-media approach appeared to be effective in preventing obesity. Two studies focused on nutrition education alone, but neither were effective in preventing obesity. Four of the twelve short-term studies focused on interventions to increase physical activity levels, and two of these studies resulted in minor reductions in overweight status in favour of the intervention. The other eight studies combined advice on diet and physical activity, but none had a significant impact. The studies were heterogeneous in terms of study design, quality, target population, theoretical underpinning, and outcome measures, making it impossible to combine study findings using statistical methods. There was an absence of cost-effectiveness data. AUTHORS' CONCLUSIONS: The majority of studies were short-term. Studies that focused on combining dietary and physical activity approaches did not significantly improve BMI, but some studies that focused on dietary or physical activity approaches showed a small but positive impact on BMI status. Nearly all studies included resulted in some improvement in diet or physical activity. Appropriateness of development, design, duration and intensity of interventions to prevent obesity in childhood needs to be reconsidered alongside comprehensive reporting of the intervention scope and process.

Adolescent↗

Post-translational modification of RelA(p65) NF-kappaB.

Stimulation with diverse agents activates the NF-kappaB (nuclear factor kappaB) transcription factor, affecting inflammatory and immune responses, proliferation, differentiation, apoptosis and tumourigenesis. Determining how NF-kappaB elicits such distinct responses is essential to understanding NF-kappaB function in diseased tissues. Recent developments illustrating that post-translational modification of NF-kappaB subunits influences their nuclear role are discussed. These observations suggest that diagnosis and new therapies based on reprogramming NF-kappaB activity could be more efficient than total NF-kappaB inhibition.

Animals↗

Interventions for treating obesity in children.

BACKGROUND: The prevalence of overweight and obesity is increasing in child populations throughout the world. Obesity in children has significant short and long term health consequences. OBJECTIVES: To assess the effects of a range of lifestyle interventions designed to treat obesity in childhood. SEARCH STRATEGY: We searched CCTR, MEDLINE, EMBASE, CINAHL, PsychLIT, Science Citation Index, Social Science Citation Index. Each database was searched from 1985 to July 2001. We also contacted experts in child obesity treatment. SELECTION CRITERIA: We selected randomised controlled trials of lifestyle interventions for treating obesity in children with a minimum of six months duration. Examples of lifestyle interventions include dietary, physical activity and/or behavioural therapy interventions, with or without the support of associated family members. Interventions from any setting and delivered by any professional were considered. However, interventions that specifically dealt with the treatment of eating disorders were excluded. DATA COLLECTION AND ANALYSIS: Two of our research team independently assessed trial quality and extracted data. Authors of the included studies were contacted for additional information where this was appropriate. MAIN RESULTS: We included 18 randomised controlled trials with 975 participants. Many studies were run from a specialist obesity clinic within a hospital setting. Five studies (n=245 participants) investigated changes in physical activity and sedentary behaviour. Two studies (n=107 participants) compared problem-solving with usual care or behavioural therapy. Nine studies (n=399 participants) compared behavioural therapy at varying degrees of family involvement with no treatment or usual care or mastery criteria and contingent reinforcement. Two studies (n=224 participants) compared cognitive behavioural therapy with relaxation.Most of the studies included in this review were too small to have the power to detect the effects of the treatment. We did not conduct a meta-analysis since so few of the trials included the same comparisons and outcomes. Therefore, we synthesised the results in a narrative format. REVIEWER'S CONCLUSIONS: Although 18 research studies were found, most of these were very small studies drawn from homogenous, motivated groups in hospital settings and so generalisable evidence from them is limited. In conclusion, there is a limited amount of quality data on the components of programs to treat childhood obesity that favour one program over another. Further research that considers psychosocial determinants for behaviour change, strategies to improve clinician-family interaction, and cost-effective programs for primary and community care is required. We conclude that no direct conclusions can be drawn from this review with confidence.

Child↗

UV stimulation induces nuclear factor kappaB (NF-kappaB) DNA-binding activity but not transcriptional activation.

The cellular response to DNA-damaging agents is partly mediated by DNA-binding transcription factors such as p53 and nuclear factor kappaB (NF-kappaB). Typically NF-kappaB activation is associated with resistance to apoptosis. Following stimulation with UV light however, NF-kappaB activation has been shown to be required for programmed cell death. To study this effect further and to determine the relationship between NF-kappaB and p53 function, we have examined the effect of UV light on U2OS cells. UV stimulation resulted in the activation of NF-kappaB DNA-binding and the induction of p53. Surprisingly, and in contrast with tumour necrosis factor alpha stimulation, this UV- induced NF-kappaB was transcriptionally inert. These observations suggest a model in which the NF-kappaB switch from an anti-apoptotic to a pro-apoptotic role within the cell results from modulation of its ability to stimulate gene expression, possibly as a result of the ability of p53 to sequester transcriptional co-activator proteins such as p300/CREB (cAMP-response-element-binding protein)-binding protein.

Animals↗

Regional localization of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) uptake: mismatch between its uptake and neurotoxic sites.

Three to 24 h following intraventricular injections of radioactive 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) into the rat, accumulations of radiolabel were widely detected, in varying degree, over neuronal perikarya in motor-related structures below the midbrain. Pretreatment with the monoamine oxidase B inhibitor pargyline largely eliminated the perikaryal radiolabeling in the substantia nigra, dorsal raphe and cerebellum, leaving that in the other regions intact. These results indicate that there exists a certain mismatch between MPTP uptake and neurotoxic sites, and that invulnerable cells can accumulate MPTP without being converted to its major active metabolite 1-methyl-4-phenylpyridine (MPP+).

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

Co-localization of tyrosine hydroxylase and glutamate decarboxylase in a subpopulation of single nigrotectal projection neurons.

The neurotransmitter phenotype(s) of nigral neurons innervating the superior colliculus (SC) in the rat was examined using a combination of immunohistochemical techniques and fluorescent retrograde tracing. After double-immunofluorescent histochemistry for tyrosine hydroxylase (TH) and glutamate decarboxylase (GAD), single cells in the rostral ventrolateral portion of the substantia nigra pars reticulata (SNr) and to a lesser extent the substantia nigra pars lateralis (SN1) displayed immunoreactivity to both antigens. Furthermore, following True blue (TB) injections into the SC and incubation for both TH and GAD immunoreactivity, a considerable number of cells in the SNr retrogradely labeled with TB (approximately 10%) were also immunopositive for both synthetic enzymes. The present study provides evidence for the coexistence of TH and GAD and thus, the coexistence of dopamine and GABA in a subpopulation of single nigrotectal projection cells.

Animals↗

Evidence for retrograde axonal transport of MPP+ in the rat.

Three to 24 h after injecting radioactive 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine ([3H]MPTP) into the rat striatum, a considerable number of neuronal perikarya were retrogradely radiolabeled in the dorsal raphe, substantia nigra pars compacta and selected regions of the substantia nigra pars reticulata, leaving cells in the ventral tegmental area unlabeled. Pretreatment with tranylcypromine prevented such radiolabel accumulation, indicating that 1-methyl-4-phenylpyridine (MPP+) (but not MPTP) undergoes selective uptake and subsequent retrograde transport in these specific striatal afferent systems.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

On the origin of the dopaminergic innervation of the paraventricular thalamic nucleus.

The origin of the dopaminergic innervation of the paraventricular thalamic nucleus was examined in the rat. Employing a combination of fluorescent retrograde tracing and immunofluorescence histochemistry for tyrosine hydroxylase, we found that this innervation predominantly takes origin from the mesencephalic A8 and A10 catecholamine cell groups.

Animals↗

Direct striatothalamic projections in the neonatal rat.

Employing anterograde axonal transport of wheat germ agglutinin conjugated to horseradish peroxidase and retrograde axonal transport of fluorescent tracers, we provided evidence for the existence of direct striatothalamic projections in the neonatal rat. The major terminal sites included the ventromedial, centrolateral and parafascicular thalamic nuclei. Cells of origin of these projections were aggregated in a mosaic fashion. The fact that such pathways do not exist in the adult suggests that they might play a transient role in the development of basal ganglia-related circuitry. These transient projections may also serve as an ideal model system to study the mechanisms underlying neuronal cell death and/or axon collateral retraction naturally occurring during the development of the nervous system.

Animals↗

Bilateral tectal projection of single nigrostriatal dopamine cells in the rat.

Employing fluorescent retrograde double/triple labeling techniques, we found that a substantial population of substantia nigra pars reticulata cells send divergent axon collaterals to both the ipsilateral striatum and bilateral superior colliculi in the rat. These multi-collateralized neurons were localized predominantly in the ventrolateral portion of the substantia nigra pars reticulata at its rostral level. Furthermore, tyrosine hydroxylase immunofluorescence histochemistry combined with fluorescent retrograde tracing techniques showed that the vast majority (more than 85%) of such specifically branched cells are dopaminergic. This novel nigral cell population seems to be in a strategic position to evoke dopamine-mediated motor impairments (i.e. abnormal saccadic eye movements in Parkinsonism) and/or behavioral syndromes (i.e. compulsive turning behavior) through the GABA-containing nigrotectal pathway.

Animals↗