Title: nicotine lozenge
Category: Medications
Created: 7/21/2022 12:00:00 AM
Last Editorial Review: 7/21/2022 12:00:00 AM

Evolving evidence suggests that nicotine may contribute to impaired asthma control by stimulating expression of nerve growth factor (NGF), a neurotrophin associated with airway remodeling and airway hyperresponsiveness. We explored the hypothesis that nicotine increases NGF by reducing lung fibroblast (LF) microRNA-98 (miR-98) and PPARγ levels, thus promoting airway remodeling. Levels of NGF, miR-98, PPARγ, fibronectin 1 (FN1), endothelin-1 (EDN1, herein referred to as ET-1), and collagen (COL1A1 and COL3A1) were measured in human LFs isolated from smoking donors, in mouse primary LFs exposed to nicotine (50 μg/ml), and in whole lung homogenates from mice chronically exposed to nicotine (100 μg/ml) in the drinking water. In selected studies, these pathways were manipulated in LFs with miR-98 inhibitor (anti-miR-98), miR-98 overexpression (miR-98 mimic), or the PPARγ agonist rosiglitazone. Compared with unexposed controls, nicotine increased NGF, FN1, ET-1, COL1A1, and COL3A1 expression in human and mouse LFs and mouse lung homogenates. In contrast, nicotine reduced miR-98 levels in LFs in vitro and in lung homogenates in vivo. Treatment with anti-miR-98 alone was sufficient to recapitulate increases in NGF, FN1, and ET-1, whereas treatment with a miR-98 mimic significantly suppressed luciferase expression in cells transfected with a luciferase reporter linked to the putative seed sequence in the NGF 3'UTR and also abrogated nicotine-induced increases in NGF, FN1, and ET-1 in LFs. Similarly, rosiglitazone increased miR-98 and reversed nicotine-induced increases in NGF, FN1, and ET-1. Taken together, these findings demonstrate that nicotine-induced increases in NGF and other markers of airway remodeling are negatively regulated by miR-98.

Title: Nicotine Can Fuel Breast Cancer, Study Suggests
Category: Health News
Created: 8/24/2010 12:10:00 PM
Last Editorial Review: 8/25/2010 12:00:00 AM

Title: Many Teens 'Vaping' for Flavor, Not Nicotine
Category: Health News
Created: 8/25/2016 12:00:00 AM
Last Editorial Review: 8/26/2016 12:00:00 AM

Title: FDA Issues Warning to Maker of Illegal Nicotine Gummies
Category: Health News
Created: 8/19/2022 12:00:00 AM
Last Editorial Review: 8/19/2022 12:00:00 AM

medlinkChildren/medlink exposed to vaping indoors absorb significantly less nicotine compared to those exposed to indoor medlinksmoking/medlink,

US teens are more likely to vape for the flavourings found in e-cigarettes rather than nicotine, suggests research published online in the journal Tobacco Control.

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The invention relates to methods of nicotine extraction from tobacco, caporal and tobacco crumb. The proposed method for extraction of nicotine from tobacco, caporal and tobacco crumb implies continuous extraction from raw material with low-boiling solvents at vapor phase followed by solvent stripper and recurrence for further reuse in the process.

(Louisiana State University Health Sciences Center) A study conducted at LSU Health New Orleans has shown for the first time that chronic exposure to inhaled nicotine alone increases blood pressure in both the body's general circulation and in the lungs that can lead to pulmonary hypertension. The study also found that nicotine-induced pulmonary hypertension is accompanied by changes in the size, shape and function (remodeling) of the blood vessels in the lung and the right lower chamber of the heart.

This study sought to determine brain nicotine kinetics from the use of increasingly popular electronic cigarettes (E-cigs). Methods: Brain uptake of nicotine following inhalation from E-cigs was directly assessed in 17 E-cig users (8 females), using ¹¹C-nicotine and positron emission tomography. The brain nicotine kinetics parameters from E-cigs were compared with those from smoking combustible cigarettes (C-cigs). Results: After inhalation of a single puff of E-cig vapor, brain nicotine concentration rose quickly (mean T1/2 27 sec) with a peak amplitude 25% higher in females than males, resembling previous observations with C-cigs. Nonetheless, brain nicotine accumulation from E-cigs was smaller than that from C-cigs in both males and females (24% and 32%, respectively). Conclusion: E-cigs can deliver nicotine rapidly to the brain. Therefore, to the extent that rapid brain uptake promotes smoking reward, e-cigarettes might maintain a degree of nicotine dependence and also serve as non-combustible substitutes for cigarettes.

Mandeep Bajaj
Dec 1, 2012; 61:3078-3080
Commentary

Nicotine addiction, through smoking, is the principal cause of preventable mortality worldwide. Human genome-wide association studies have linked polymorphisms in the CHRNA5-CHRNA3-CHRNB4 gene cluster, coding for the α5, α3, and β4 nicotinic acetylcholine receptor (nAChR) subunits, to nicotine addiction. β4*nAChRs have been implicated in nicotine withdrawal, aversion, and reinforcement. Here we show that β4*nAChRs also are involved in non-nicotine-mediated responses that may predispose to addiction-related behaviors. β4 knock-out (KO) male mice show increased novelty-induced locomotor activity, lower baseline anxiety, and motivational deficits in operant conditioning for palatable food rewards and in reward-based Go/No-go tasks. To further explore reward deficits we used intracranial self-administration (ICSA) by directly injecting nicotine into the ventral tegmental area (VTA) in mice. We found that, at low nicotine doses, β4KO self-administer less than wild-type (WT) mice. Conversely, at high nicotine doses, this was reversed and β4KO self-administered more than WT mice, whereas β4-overexpressing mice avoided nicotine injections. Viral expression of β4 subunits in medial habenula (MHb), interpeduncular nucleus (IPN), and VTA of β4KO mice revealed dose- and region-dependent differences: β4*nAChRs in the VTA potentiated nicotine-mediated rewarding effects at all doses, whereas β4*nAChRs in the MHb-IPN pathway, limited VTA-ICSA at high nicotine doses. Together, our findings indicate that the lack of functional β4*nAChRs result in deficits in reward sensitivity including increased ICSA at high doses of nicotine that is restored by re-expression of β4*nAChRs in the MHb-IPN. These data indicate that β4 is a critical modulator of reward-related behaviors.

SIGNIFICANCE STATEMENT Human genetic studies have provided strong evidence for a relationship between variants in the CHRNA5-CHRNA3-CHRNB4 gene cluster and nicotine addiction. Yet, little is known about the role of β4 nicotinic acetylcholine receptor (nAChR) subunit encoded by this cluster. We investigated the implication of β4*nAChRs in anxiety-, food reward- and nicotine reward-related behaviors. Deletion of the β4 subunit gene resulted in an addiction-related phenotype characterized by low anxiety, high novelty-induced response, lack of sensitivity to palatable food rewards and increased intracranial nicotine self-administration at high doses. Lentiviral vector-induced re-expression of the β4 subunit into either the MHb or IPN restored a "stop" signal on nicotine self-administration. These results suggest that β4*nAChRs provide a promising novel drug target for smoking cessation.

Infantile colic affects almost 10% of all infants and is characterized by crying and fussing in an otherwise healthy and well-fed infant. Prenatal exposure to tobacco smoking is a risk factor, but it is unclear whether nicotine causes the association.

Infants exposed to nicotine replacement therapy during pregnancy had elevated infantile colic risk of the same magnitude as infants exposed to tobacco smoking. Intrauterine exposure to nicotine may play a causal role in the pathogenesis of infantile colic. (Read the full article)

Little is known about the impact of tobacco smoke exposure on preterm children with bronchopulmonary dysplasia. It is essential to understand how environmental exposures, such as tobacco smoke, influence respiratory morbidities in this vulnerable population.

Chronic tobacco smoke exposure is common in children with bronchopulmonary dysplasia. In children who required home respiratory support, hair nicotine levels were a better predictor of hospitalization and activity limitation than caregiver self-report. (Read the full article)

Smoking has been found to increase the risk of some specific congenital anomalies; however, results remain inconsistent. Nicotine replacement therapy (NRT) is increasingly being used as for smoking cessation in pregnancy although little is known about its association with congenital anomalies.

Being prescribed NRT while pregnant was not associated with major congenital anomalies (MCA), except a small increase in respiratory anomalies (3/1000 births). This must be considered in context of the rarity of MCAs and higher morbidities in the NRT group. (Read the full article)

Title: Magnetic Brain Stimulation May Temporarily Dull Nicotine Craving
Category: Health News
Created: 4/26/2013 12:36:00 PM
Last Editorial Review: 4/29/2013 12:00:00 AM

Chronic nicotine inhalation modifies both systemic and pulmonary blood pressure, with the latter accompanied by right ventricular remodeling, possibly

Initial observations showed that an ingredient in tobacco, probably nicotine, could put smokers at a lower risk of getting the disease. The researchers

Breastfeeding mothers who use e-cigarettes or nicotine replacement therapies may be putting their breastfed babies at higher risk for skull defects, reports a new study.

Stimulant given as ‘likely’ reason for lower infections but authorities stress health risks

Legal marijuana producers also report spike in demand during lockdown