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Healthy Non-smokers (healthy + non-smoker)

Distribution by Scientific Domains

Medical Sciences	50%

Selected Abstracts

IMAGING STUDY: Exposure to smoking cues during an emotion recognition task can modulate limbic fMRI activation in cigarette smokers

ADDICTION BIOLOGY, Issue 4 2009
Eric Artiges
ABSTRACT Smoking cues (SCs) refer to smoking-associated environmental stimuli that may trigger craving and withdrawal symptoms, and predispose to relapse in smokers. Although previous brain imaging studies have explored neural responses to SCs, no study has characterized the effects of SCs on cerebral activity in smokers engaged in an attention-demanding cognitive task that is unrelated to smoking. Thirteen tobacco smokers and a demographically matched group of 13 healthy non-smokers participated in a fast event-related functional magnetic resonance imaging (fMRI) study that involved a visual task integrating SCs and neutral cues (NCs) during emotion recognition trials requiring a high level of attention. No significant SC-induced alterations were detected in smokers' behavioural performance. fMRI results show that non-smokers exhibited no difference between SC and NC trials; in contrast, smokers showed SC-induced widespread deactivations in a limbic, paralimbic and striatal network classically involved in addiction, and activation in the right dorsolateral prefrontal cortex. In addition, a correlation between deactivation of the right insula and the severity of smoking dependence (Fagerström test) was detected in smokers. These results suggest that the neural reactivity of smokers to SCs can be modified in the context of a cognitive challenge. This could reflect smokers' ability to inhibit cue-induced craving and may help in smoking cessation. [source]

Predictive value of clinical and microbiological parameters for the treatment outcome of scaling and root planing

JOURNAL OF CLINICAL PERIODONTOLOGY, Issue 7 2005
P. F. Brochut
Abstract Objectives: To compare the clinical and microbiological outcome of non-surgical periodontal therapy after 6 months with data obtained after hygienic phase or 6 weeks after completion of non-surgical therapy, in order to evaluate the value of clinical and microbiological parameters to predict treatment success. Material and Methods: Clinical and microbiological data were available from 271 sites in 10 systemically healthy non-smokers with moderate-to-advanced chronic periodontal disease (24,32 sites per individual). Subgingival plaque samples were tested for the presence of Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Tannerella forsythensis and Treponema denticola using RNA probes. Results: Stepwise multiple linear regression analysis revealed a significant impact of the number of sites with visible plaque index >1 after hygienic phase on the bleeding tendency of a subject at month 6 (p<0.01). Furthermore, an association could be demonstrated between the number of residual pockets (PD>3 mm) 6 months after therapy and the number of bleeding sites and suppurating sites after hygienic phase (p=0.016). Six weeks after therapy, the mean total bacterial loads had a significant impact on the bleeding tendency of a subject at month 6 (p<0.01). Although the average numbers of sites with persisting P. gingivalis, A. actinomycetemcomitans, T. forsythensis and T. denticola seemed to be very similar 6 weeks and 6 months after therapy, large variations were noted between subjects, and therefore the microbiological status of a subject at week 6 could not predict the status at month 6. Conclusions: The present study showed a limited potential of microbiological tests, performed after hygienic phase or shortly after non-surgical periodontal therapy, to predict the clinical outcome 6 months later, but confirmed the importance of an establishment of perfect oral hygiene before non-surgical therapy. [source]

Analysis of exhaled breath from smokers, passive smokers and non-smokers by solid-phase microextraction gas chromatography/mass spectrometry

BIOMEDICAL CHROMATOGRAPHY, Issue 5 2009
Bogus, aw Buszewski
Abstract In this study, 38 samples of expired air were collected and analyzed from 20 non-smoking volunteers, four passive smokers and 14 smokers (21 women and 17 men). Measurements were carried out using solid-phase microextraction (SPME) as an isolation and preconcentration technique. The determination and identification were accomplished by gas chromatography coupled with mass spectrometry (GC/MS). Our data showed that ca 32% of all identified compounds in the breath of healthy non-smokers were saturated hydrocarbons. In the breath of smoking and passive smoking volunteers hydrocarbons were predominant, but also present were more exogenous analytes such as furan, acetonitrile and benzene than in the breath of non-smokers. Acetonitrile, furan, 3-methylfuran, 2,5-dimethylfuran, 2-butanone, octane and decane were identified in breath of smoking and passive smoking persons. Copyright © 2008 John Wiley & Sons, Ltd. [source]

Glucocorticoid sensitivity of lipopolysaccharide-stimulated chronic obstructive pulmonary disease alveolar macrophages

CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 1 2009
J. Armstrong
Summary It has been reported that alveolar macrophages from patients with chronic obstructive pulmonary disease (COPD) display glucocorticoid (Gc) resistance. The Gc sensitivity of inflammatory mediators released by COPD macrophages may vary. The objective of this study was to identify Gc-insensitive inflammatory mediators produced by lipopolysaccharide (LPS)-stimulated alveolar macrophages from COPD patients. LPS-stimulated alveolar macrophages from 15 COPD patients, nine smokers (S) and nine healthy non-smokers (HNS) were stimulated with LPS with or without dexamethasone (100 and 1000 nM). Luminex and enzyme-linked immunosorbent assay were used to measure 23 inflammatory mediators. After LPS stimulation there were lower levels of inflammatory mediators in COPD patients and S compared to HNS. There was no difference between groups for the effects of dexamethasone at either concentration (P > 0·05 for all comparisons). Tumour necrosis factor (TNF)-,, interleukin (IL)-6 and growth-related oncogene (GRO)-, displayed the greatest sensitivity to dexamethasone in COPD patients, while IL-8, granulocyte,macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) were the least sensitive. COPD macrophages have a reduced response to LPS. Gc sensitivity was similar in COPD macrophages compared to controls. We identify some Gc-insensitive cytokines, including GM-CSF, G-CSF and IL-8, that may be involved in the progression of airway inflammation in COPD patients. [source]