Smoking Cessation

Rennard, Stephen I.; Daughton, David M.

doi:10.1016/j.ccm.2013.11.002

Cited by 24 publications

(16 citation statements)

References 68 publications

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“…After at least a week of chronic nicotine administration in mice, cessation of nicotine exposure or administration of a nAChR antagonist induces affective, somatic, and cognitive signs of withdrawal (Malin et al 1994; De Biasi and Salas 2008). The withdrawal syndrome exhibited can be alleviated by nicotine administration—akin to nicotine replacement strategies such as nicotine patches or gum—or by administration of pharmacological agents used as cessation aids in humans, such as bupropion or varenicline (Rennard and Daughton 2014). Because mice express neuroadaptations that result in the nicotine withdrawal syndrome, and because nAChR subunit knockout mouse lines are readily available, researchers have been able to study the functional contributions of particular nAChR subunits to specific symptoms of withdrawal.…”

Section: Withdrawal Syndrome In Micementioning

confidence: 99%

Nicotine Withdrawal

McLaughlin¹,

Dani²,

Biasi³

2015

Current Topics in Behavioral Neurosciences

127

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An aversive abstinence syndrome manifests 4–24 h following cessation of chronic use of nicotine-containing products. Symptoms peak on approximately the 3rd day and taper off over the course of the following 3–4 weeks. While the severity of withdrawal symptoms is largely determined by how nicotine is consumed, certain short nucleotide polymorphisms (SNPs) have been shown to predispose individuals to consume larger amounts of nicotine more frequently—as well as to more severe symptoms of withdrawal when trying to quit. Additionally, rodent behavioral models and transgenic mouse models have revealed that specific nicotinic acetylcholine receptor (nAChR) subunits, cellular components, and neuronal circuits are critical to the expression of withdrawal symptoms. Consequently, by continuing to map neuronal circuits and nAChR subpopulations that underlie the nicotine withdrawal syndrome—and by continuing to enumerate genes that predispose carriers to nicotine addiction and exacerbated withdrawal symptoms—it will be possible to pursue personalized therapeutics that more effectively treat nicotine addiction.

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Section: Withdrawal Syndrome In Micementioning

confidence: 99%

Nicotine Withdrawal

McLaughlin¹,

Dani²,

Biasi³

2015

Current Topics in Behavioral Neurosciences

127

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“…Preventing CS-related diseases can be best achieved by avoiding smoking initiation [3]; however, when the smoking habit has already started, smoking cessation considerably decreases numerous adverse health effects [4]. Intervention by smoking cessation during the early stages of COPD can decrease the rate of lung-function loss [5].…”

Section: Introductionmentioning

confidence: 99%

Regional heterogeneity in response of airway epithelial cells to cigarette smoke

et al. 2018

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BackgroundCigarette smoke (CS) exposure causes an abnormal inflammatory response, which can result in chronic obstructive pulmonary disease (COPD). Previous studies show that this disorder predominantly occurs in peripheral or small-airway areas, whereas the same condition has not been identified in the larger airways during the course of COPD. However, the different biochemical and genetic alterations occurring in response to CS exposure among airway epithelial cells from different sites in the lungs have not been fully investigated.MethodsHuman small airway epithelial cells (SAECs) and normal human bronchial epithelial cells (NHBEs) were exposed to CS extract (CSE), and microarray analysis was used to determine gene- and protein-expression profiles and identify alterations following CSE exposure in both cell types. An in vivo smoking experiment was also performed to confirm differential responses to CS between sites in the lung.ResultsMicroarray analysis of SAECs and NHBEs following 24 h of CSE exposure showed that inflammatory related pathways and terms, including the tumor necrosis factor-signaling pathway, were overrepresented, especially in SAECs. Clustering analysis highlighted prostaglandin-endoperoxide synthase-2 [also known as cyclooxygenase (COX)-2] as a gene specifically upregulated in SAECs, with COX-2 mRNA and protein expression significantly elevated by CSE exposure in SAECs (3.1- and 3.1-fold, respectively), but not in NHBEs. Furthermore, time-course analysis of COX-2 expression revealed earlier increases in SAECs compared with NHBEs following CS exposure. Short-term exposure of mouse lungs to CS was found to predominantly induce COX-2 expression in the small airway.ConclusionsThe small airway is more susceptible to CSE than the large airway and could be the initial site of development of CS-related respiratory diseases, such as COPD.Electronic supplementary materialThe online version of this article (10.1186/s12890-018-0715-4) contains supplementary material, which is available to authorized users.

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“…3 Relapse is common during smoking cessation attempts. 4,5 Social support interventions, which involve a person's close social relationships, have been shown to be important in preventing relapse. 5 Developing effective network interventions to reduce smoking requires a greater understanding of the range of social network influences beyond social support that might be leveraged to encourage cessation and prevent relapse.…”

mentioning

confidence: 99%