Relevant bibliographies by topics / Nicotine

Academic literature on the topic 'Nicotine'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 July 2024

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Journal articles on the topic "Nicotine"

Zenkner, Fernanda Fleig, Márcia Margis-Pinheiro, and Alexandro Cagliari. "Nicotine Biosynthesis in Nicotiana: A Metabolic Overview." Tobacco Science 56, no. 1 (April 1, 2019): 1–9. http://dx.doi.org/10.3381/18-063.

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Alkaloids are important compounds found in Nicotiana plants, essential in plant defense against herbivores. The main alkaloid of Nicotiana tabacum, nicotine, is produced in roots and translocated to the leaves. Nicotine is formed by a pyrrolidine and a pyridine ring in a process involving several enzymes. The pyridine ring of nicotine is derived from nicotinic acid, whereas the pyrrolidine ring originates from polyamine putrescine metabolism. After synthesis in root cortical cells, a set of transporters is known to transport nicotine upward to the aerial part and store it in leaf vacuoles. Moreover, nicotine can be metabolized in leaves, giving rise to nornicotine through the N-demethylation process. Some Nicotiana wild species produce acyltransferase enzymes, which allow the plant to make N-acyl-nornicotine, an alkaloid with more potent insecticidal properties than nicotine. However, although we can find a wealth of information about the alkaloid production in Nicotiana spp., our understanding about nicotine biosynthesis, transport, and metabolism is still incomplete. This review will summarize these pathways on the basis on recent literature, as well as highlighting questions that need further investigation.

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Page, Stephen J., Mingyan Zhu, and Suzanne M. Appleyard. "Effects of acute and chronic nicotine on catecholamine neurons of the nucleus of the solitary tract." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 316, no. 1 (January 1, 2019): R38—R49. http://dx.doi.org/10.1152/ajpregu.00344.2017.

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Nicotine is an addictive drug that has broad effects throughout the brain. One site of action is the nucleus of the solitary tract (NTS), where nicotine initiates a stress response and modulates cardiovascular and gastric function through nicotinic acetylcholine receptors (nAChRs). Catecholamine (CA) neurons in the NTS influence stress and gastric and cardiovascular reflexes, making them potential mediators of nicotine’s effects; however nicotine’s effect on these neurons is unknown. Here, we determined nicotine’s actions on NTS-CA neurons by use of patch-clamp techniques in brain slices from transgenic mice expressing enhanced green fluorescent protein driven by the tyrosine hydroxylase promoter (TH-EGFP). Picospritzing nicotine both induced a direct inward current and increased the frequency of spontaneous excitatory postsynaptic currents (sEPSCs) in NTS-CA neurons, effects blocked by nonselective nAChR antagonists TMPH and MLA. The increase in sEPSC frequency was mimicked by nAChRα7 agonist AR-R17779 and blocked by nAChRα7 antagonist MG624. AR-R17779 also increased the firing of TH-EGFP neurons, an effect dependent on glutamate inputs, as it was blocked by the glutamate antagonist NBQX. In contrast, the nicotine-induced current was mimicked by nAChRα4β2 agonist RJR2403 and blocked by nAChRα4β2 antagonist DHβE. RJR2403 also increased the firing rate of TH-EGFP neurons independently of glutamate. Finally, both somatodendritic and sEPSC nicotine responses from NTS-CA neurons were larger in nicotine-dependent mice that had under gone spontaneous nicotine withdrawal. These results demonstrate that 1) nicotine activates NTS-CA neurons both directly, by inducing a direct current, and indirectly, by increasing glutamate inputs, and 2) NTS-CA nicotine responsiveness is altered during nicotine withdrawal.

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Liu, Zhi, Yo Otsu, Cristina Vasuta, Hiroyuki Nawa, and Timothy H. Murphy. "Action-Potential-Independent GABAergic Tone Mediated by Nicotinic Stimulation of Immature Striatal Miniature Synaptic Transmission." Journal of Neurophysiology 98, no. 2 (August 2007): 581–93. http://dx.doi.org/10.1152/jn.00768.2006.

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Stimulation of presynaptic nicotinic acetylcholine receptors (nAChRs) increases the frequency of miniature excitatory synaptic activity (mEPSCs) to a point where they can promote cell firing in hippocampal CA3 neurons. We have evaluated whether nicotine regulation of miniature synaptic activity can be extended to inhibitory transmission onto striatal medium spiny projection neurons (MSNs) in acute brain slices. Bath application of micromolar nicotine typically induced 12-fold increases in the frequency of miniature inhibitory synaptic currents (mIPSCs). Little effect was observed on the amplitude of mIPSCs or mEPSCs under these conditions. Nicotine stimulation of mIPSCs was dependent on entry of extracellular calcium because removal of calcium from perfusate was able to block its action. To assess the potential physiological significance of the nicotine-stimulated increase in mIPSC frequency, we also examined the nicotine effect on evoked IPSCs (eIPSCs). eIPSCs were markedly attenuated by nicotine. This effect could be attributed to two potential mechanisms: transmitter depletion due to extremely high mIPSC rates and/or a reduction in presynaptic excitability associated with nicotinic depolarization. Treatment with low concentrations of K+ was able to in part mimic nicotine's stimulatory effect on mIPSCs and inhibitory effect on eIPSCs. Current-clamp recordings confirmed a direct depolarizing action of nicotine that could dampen eIPSC activity leading to a switch to striatal inhibitory synaptic transmission mediated by tonic mIPSCs.

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DeVito, Elise E., Kevin P. Jensen, Stephanie S. O’Malley, Ralitza Gueorguieva, Suchitra Krishnan-Sarin, Gerald Valentine, Peter I. Jatlow, and Mehmet Sofuoglu. "Modulation of “Protective” Nicotine Perception and Use Profile by Flavorants: Preliminary Findings in E-cigarettes." Nicotine & Tobacco Research 22, no. 5 (April 17, 2019): 771–81. http://dx.doi.org/10.1093/ntr/ntz057.

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Abstract Introduction Characterizing flavors are widely available in e-cigarettes and motivate initiation and continued use. Flavors may enhance appeal and facilitate development of addiction to tobacco products through modulation of tobacco products’ reinforcing or aversive actions. Palatable flavors (eg, fruit) may increase appeal through primary reinforcing properties. Menthol’s cooling and anesthetic effects may increase appeal by counteracting nicotine’s aversive effects. Genetics provide a method for modeling individual differences in sensitivity to nicotine’s effects. A common polymorphism, rs16969968, encoded in the α5 nicotinic acetylcholine receptor subunit gene (CHRNA5), is a well-recognized marker for smoking risk and reduces sensitivity to nicotine aversiveness. Methods This pilot study tested how flavors impacted e-cigarette appeal and self-administration. In a single testing day, cigarette smokers (N = 32; 94% menthol-smokers) self-administered e-cigarettes containing e-liquids differing in nicotine level (0 mg/mL, 24 mg/mL) and flavor (unflavored, menthol, fruit-flavored) within directed and ad libitum e-cigarette paradigms. Subjective drug effects, number of puffs, rs16969968 genotype, plasma nicotine, and menthol glucuronide levels were collected. Results Menthol partially ameliorated nicotine aversiveness; fruit did not. In nicotine’s absence, fruit flavor increased self-reported preference and ad libitum use relative to menthol-containing or unflavored e-liquids. Individuals with high-smoking-risk rs16969968 genotype (N = 7) reported greater craving alleviation following directed administration of nicotine-containing e-liquids, showed a trend rating nicotine-containing e-liquids as less harsh, and self-administered more nicotine during ad libitum compared to individuals with low-smoking-risk genotype (N = 23). Conclusions While menthol countered aversiveness of nicotine-containing e-liquids, fruit flavor increased appeal of nicotine-free e-liquids. These preliminary findings suggest menthol and fruit flavor increase e-cigarettes’ appeal through distinct mechanisms. Implications This study provides a detailed characterization of the effects of flavors (unflavored, menthol, fruit), nicotine (0 mg/mL, 24 mg/mL) and their interactions on the subjective drug effects and ad libitum self-administration of e-cigarettes. Genetics were used to assess these effects in higher-smoking-risk (diminished sensitivity to nicotine aversiveness) and lower-risk groups. Findings could inform impact of regulation of flavors or nicotine in e-cigarettes, and their impacts on vulnerable sub-populations.

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Sansone, Luigi, Francesca Milani, Riccardo Fabrizi, Manuel Belli, Mario Cristina, Vincenzo Zagà, Antonio de Iure, Luca Cicconi, Stefano Bonassi, and Patrizia Russo. "Nicotine: From Discovery to Biological Effects." International Journal of Molecular Sciences 24, no. 19 (September 26, 2023): 14570. http://dx.doi.org/10.3390/ijms241914570.

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Nicotine, the primary psychoactive agent in tobacco leaves, has led to the widespread use of tobacco, with over one billion smokers globally. This article provides a historical overview of tobacco and discusses tobacco dependence, as well as the biological effects induced by nicotine on mammalian cells. Nicotine induces various biological effects, such as neoangiogenesis, cell division, and proliferation, and it affects neural and non-neural cells through specific pathways downstream of nicotinic receptors (nAChRs). Specific effects mediated by α7 nAChRs are highlighted. Nicotine is highly addictive and hazardous. Public health initiatives should prioritize combating smoking and its associated risks. Understanding nicotine’s complex biological effects is essential for comprehensive research and informed health policies. While potential links between nicotine and COVID-19 severity warrant further investigation, smoking remains a significant cause of morbidity and mortality globally. Effective public health strategies are vital to promote healthier lifestyles.

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Grieder, Taryn E., Morgane Besson, Geith Maal-Bared, Stéphanie Pons, Uwe Maskos, and Derek van der Kooy. "β2* nAChRs on VTA dopamine and GABA neurons separately mediate nicotine aversion and reward." Proceedings of the National Academy of Sciences 116, no. 51 (November 27, 2019): 25968–73. http://dx.doi.org/10.1073/pnas.1908724116.

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Evidence shows that the neurotransmitter dopamine mediates the rewarding effects of nicotine and other drugs of abuse, while nondopaminergic neural substrates mediate the negative motivational effects. β2* nicotinic acetylcholine receptors (nAChR) are necessary and sufficient for the experience of both nicotine reward and aversion in an intra-VTA (ventral tegmental area) self-administration paradigm. We selectively reexpressed β2* nAChRs in VTA dopamine or VTA γ-amino-butyric acid (GABA) neurons in β2−/−mice to double-dissociate the aversive and rewarding conditioned responses to nicotine in nondependent mice, revealing that β2* nAChRs on VTA dopamine neurons mediate nicotine’s conditioned aversive effects, while β2* nAChRs on VTA GABA neurons mediate the conditioned rewarding effects in place-conditioning paradigms. These results stand in contrast to a purely dopaminergic reward theory, leading to a better understanding of the neurobiology of nicotine motivation and possibly to improved therapeutic treatments for smoking cessation.

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Kedmi, Merav, Arthur L. Beaudet, and Avi Orr-Urtreger. "Mice lacking neuronal nicotinic acetylcholine receptor β4-subunit and mice lacking both α5- and β4-subunits are highly resistant to nicotine-induced seizures." Physiological Genomics 17, no. 2 (April 13, 2004): 221–29. http://dx.doi.org/10.1152/physiolgenomics.00202.2003.

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Nicotine, the main addictive component of tobacco, evokes a wide range of dose-dependent behaviors in rodents, and when administrated in high doses, it can induce clonic-tonic seizures. Nicotine acts through the nicotinic acetylcholine receptors (nAChRs). Mutations in the human α4- and the β2-nAChR subunit genes cause autosomal dominant nocturnal frontal lobe epilepsy. Using transgenic mice with mutations in nAChR subunits, it was demonstrated previously that the α4-, α5-, and α7-subunits are involved in nicotine-induced seizures. To examine the possibility that the β4-subunit is also involved in this phenotype, we tested mice with homozygous β4-subunit deficiency. The β4 null mice were remarkably resistant to nicotine-induced seizures compared with wild-type and α5 null mice. We also generated mice with double deficiency of both α5- and β4-nAChR subunits and demonstrated that they were more resistant to nicotine’s convulsant effect than either the α5 or the β4 single mutant mice. In addition, the single α5 mutants and the double α5β4-deficient mice exhibited a significantly shorter latency time to seizure than that of the wild-type mice. Our results thus show that β4-containing nAChRs have a crucial role in the pathogenesis of nicotine-induced seizures. Furthermore, by comparing multiple mutant mice with single and double subunit deficiency, we suggest that nicotinic receptors containing either α5- or β4-subunits are involved in nicotine-induced seizures and that receptors containing both subunits are likely to contribute to this phenomena as well. However, the α5-subunit, but not the β4-subunit, regulates the rate of response to high doses of nicotine.

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Kizawa, Yasuo, Michiko Shinkai, and Issei Takayanagi. "Effects of chronic nicotine treatment on nicotinic receptors in the rabbit urinary bladder." Canadian Journal of Physiology and Pharmacology 68, no. 1 (January 1, 1990): 99–103. http://dx.doi.org/10.1139/y90-015.

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Nicotine induced a phasic contraction in the rabbit urinary bladder. The response was abolished by hexamethonium and partially reduced by atropine and capsaicin. Simultaneous atropine and capsaicin treatment did not abolish the contraction. These findings suggest that the response to nicotine is due to acetylcholine, tachykinins, and unknown mediator release. In contrast, nicotine-induced contraction diminished following the chronic nicotine treatment without a change of its pharmacological properties. These results suggest the possibility that chronic nicotine treatment causes a decrease in nicotinic receptor numbers. Therefore, the binding properties of (−)-[3H]nicotine on rabbit urinary detrusor muscle membrane fractions were studied to evaluate the effects of chronic nicotine treatment on nicotinic receptors. Specific (−)-[3H]nicotine binding reached saturation and Scatchard plots were curvilinear, suggesting the existence of two different affinity sites for (−)-[3H]nicotine. Dissociation constants (KD) and maximum binding sites (Bmax) were KD1 = 4.91 ± 1.88 nM, Bmax1 = 2.42 ± 0.22 fmol/mg protein and KD2 = 263 ± 56 nM, Bmax2 = 25.0 ± 4.3 fmol/mg protein. In urinary bladder membrane fractions from chronic nicotine-treated rabbits, KD and Bmax values were KD1 = 3.96 ± 0.38 nM, Bmax1 = 1.07 ± 0.25 fmol/mg protein and KD2 = 249 ± 12 nM, Bmax2 = 10.8 ± 1.5 fmol/mg protein. Dissociation constants for both sites following chronic nicotine treatment did not change but maximum binding site numbers for both sites significantly decreased (p < 0.05). These results suggest that the decrease in contractile response evoked by nicotine after chronic nicotine treatment in rabbit urinary bladder is due to a decrease in numbers of nicotinic receptors.Key words: nicotine, rabbit urinary bladder, nicotinic receptors.

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Bhanu Prakash G, Rajagopalan Vijayaraghavan, Senthilkumar Sivanesan, and Madhankumar Swaminathan. "A study on the agents that reduces the nicotine induced nicotinic receptor density in wistar rats." International Journal of Research in Pharmaceutical Sciences 12, no. 1 (January 6, 2021): 430–35. http://dx.doi.org/10.26452/ijrps.v12i1.4074.

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The most important substance causing addiction towards cigarette is nicotine. Nicotine abstinence causes withdrawal symptoms in smokers. It is not just nicotine, along with it is the upregulation of nicotinic receptor density (NRD) that leads to addiction. All together makes nicotine deaddiction the most difficult aspect. Nicotine receptor density increases as long as the person is exposed to nicotine. When once the NRD is initiated by nicotine, later though you stop smoking, the increased nicotine receptors create an urge to smoke. Hence the person feels to smoke for satisfying the nicotine receptors. The smokers may attempt to quit smoking but the NRD will create an urge for nicotine again. One cannot completely quit smoking or cannot stop taking nicotine, until the NRD is reduced to normal. In our present study we have studied the effect of citric acid and tyrosine on decreasing nicotinic receptor density. We have induced the nicotinic receptor density to raise and studied the citric acid and tyrosine’s effect in maintaining the NRD closer to normal. The study concludes that citric acid and tyrosine have reduced the NRD significantly. This can control withdrawal symptoms and can stop craving for nicotine and finally can lead to cessation of smoking and from taking nicotine therapy.

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Wongtrakool, Cherry, Susanne Roser-Page, Hilda N. Rivera, and Jesse Roman. "Nicotine alters lung branching morphogenesis through the α7 nicotinic acetylcholine receptor." American Journal of Physiology-Lung Cellular and Molecular Physiology 293, no. 3 (September 2007): L611—L618. http://dx.doi.org/10.1152/ajplung.00038.2007.

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There is abundant epidemiological data linking prenatal environmental tobacco smoke with childhood asthma and wheezing, but the underlying molecular and physiological mechanisms that occur in utero to explain this link remain unelucidated. Several studies suggest that nicotine, which traverses the placenta, is a causative agent. Therefore, we studied the effects of nicotine on lung branching morphogenesis using embryonic murine lung explants. We found that the expression of α7 nicotinic acetylcholine receptors, which mediate many of the biological effects of nicotine, is highest in pseudoglandular stage lungs compared with lungs at later stages. We then studied the effects of nicotine in the explant model and found that nicotine stimulated lung branching in a dose-dependent fashion. α-Bungarotoxin, an antagonist of α7 nicotinic acetylcholine receptors, blocked the stimulatory effect of nicotine, whereas GTS-21, a specific agonist, stimulated branching, thereby mimicking the effects of nicotine. Explants deficient in α7 nicotinic acetylcholine receptors did not respond to nicotine. Nicotine also stimulated the growth of the explant. Altogether, these studies suggest that nicotine stimulates lung branching morphogenesis through α7 nicotinic acetylcholine receptors and may contribute to dysanaptic lung growth, which in turn may predispose the host to airway disease in the postnatal period.

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Dissertations / Theses on the topic "Nicotine"

Harrington, Lauriane. "The role of β4-containing nicotinic acetylcholine receptors in nicotine addiction." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066328/document.

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Le tabac est consommé par environ un milliard de personnes. D'après l'Organisation Mondiale de la Santé, le tabagisme est la première cause évitable de mortalité dans le monde, provocant six millions de morts par an. La nicotine est le composant neuro-actif principal dans le tabac, et exerce ses effets neurologiques via une activation directe des récepteurs nicotiniques de l’acétylcholine (nAChR). Ces récepteurs transmembranaires sont composés de sous-unités alpha, ou alpha plus beta, créant une variété de canaux ioniques ligand-dépendants activés par le neurotransmetteur ACh. Les études génétiques chez l’homme ont mis en évidence des variants dans le cluster génomique CHRNA5-CHRNA3-CHRNB4, codant pour les sous-unités α5, α3 et β4, comme facteurs influençant le tabagisme. Cette thèse a étudié le rôle des nAChRs contenant la sous-unité β4 (β4*) dans l’addiction à la nicotine. En collaboration, nous avons montré que les souris déficientes pour la sous-unité β4 (β4 KO), sont moins sensibles aux effets récompensant et aversifs de la nicotine. En générant un lentivirus exprimant la séquence murine d'ADN complémentaire de β4, j’ai pu restaurer son expression dans des régions d’intérêt du cerveau, sur un fond génétique β4KO. Ceci a permis de mettre en évidence le rôle du réseau habénulo-interpedonculaire dans la contribution des β4* nAChRs à la consommation de nicotine. Ceci a également démontré le rôle modulateur de ces récepteurs dans les réponses de la voie mésolimbique à la nicotine, voie centrale dans l'effet renforçant des drogues
Tobacco is consumed by an estimated 1 billion people world-wide. The World Health Organization names tobacco consumption the primary cause of preventable morbidity and mortality, causing six million deaths per year. Nicotine is the principal neuro-active compound in tobacco, and exerts neurological effects by binding to nicotinic acetylcholine receptors (nAChRs). These transmembrane receptors are composed of alpha or alpha plus beta subunits, forming a diverse variety of ligand-gated ion channels endogenously activated by ACh. Human genetic studies have highlighted variants in the CHRNA5-CHRNA3-CHRNB4 genomic cluster, coding for subunits α5, α3 and β4, as altering smoking behaviours. The present thesis investigated the role of β4-containing (β4*) nAChRs in nicotine addiction. In collaboration, we showed that β4 knockout (KO) mice are less sensitive to nicotine reward and nicotine aversion. Generating a lentivirus for the expression of mouse β4 nAChR subunit complementary DNA, I was able to restore receptor expression to brain regions of interest on a KO background, locating the role of β4* nAChR in nicotine reward and aversion to the habenulo-interpedunular pathway. This also demonstrated the receptor’s modulation of nicotinic responses of the mesolimbic system, central hub of drug reinforcement

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Munhoz, Egberto [UNESP]. "Administração subcrônica de nicotina modifica as respostas neuroendócrina e neuroquímica induzidas pelo teste de natação forçada." Universidade Estadual Paulista (UNESP), 2010. http://hdl.handle.net/11449/104039.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
O estresse, atualmente, é considerado um fator importante na fisiopatologia de muitos distúrbios psiquiátricos. Embora os efeitos do estresse agudo possam ser contrabalanceados por respostas adaptativas, o estresse intenso, repetido ou prolongado pode eliciar alterações neuronais duradouras que constituirão as bases de doenças psiquiátricas, como a depressão. Levantamentos epidemiológicos também mostram elevada prevalência de tabagistas entre pacientes com depressão maior. Estas altas taxas de comorbidade sugerem uma provável relação causal: pacientes com depressão proeminente procurariam a nicotina para alívio dos sintomas. Assim, este trabalho investigou as alterações neuroquímicas e neuroendócrinas mediadas pela nicotina na resposta de adaptação ao estresse, utilizando-se, para tanto, o teste modificado da natação forçada (TNF). Para tanto, ratos Wistar machos foram submetidos ao TNF (30 cm de água, 24 ± 1ºC) por 15 min e tratados (1, 19 e 23h) com nicotina (NIC: 0,5 mg/kg, sc), imipramina (IMI: 15 mg/kg, ip) ou salina (SAL). Uma hora após a última injeção, os animais foram reexpostos (5 min) à mesma cuba. Imediatamente após o teste, os animais foram sacrificados; o hipocampo dorsal (HD) e ventral (HV), hipotálamo (HT) e os núcleos dorsal (DR) e mediano (MR) da rafe foram coletados por punch para quantificação de 5-HT, 5-HIAA e NA por HPLC e o sangue, para quantificação da corticosterona plasmática por radioimunoensaio. O hipocampo total também foi utilizado para avaliar a expressão do receptor serotoninérgico 5-HT1A e do glicorreceptor (GR) por western blot. Ainda, avaliou-se o efeito da prazosina nas alterações neuroquímicas induzidas pelo TNF. O tratamento subcrônico com NIC e IMI reduziu em 39% e 50%, respectivamente, o parâmetro de imobilidade e aumentou em 52% e 66%, respectivamente, as contagens de escalada, em relação ao grupo...
Stress is considered a key component in the pathophysiology of several psychiatric diseases. Although the effects of acute stress can be counterbalanced by adaptative responses, intense, repeated or prolonged stress can elicit long lasting neuronal alterations that are related to the occurrence of psychiatric disorders, such as depression. Epidemiological studies have also identified a high prevalence of smokers among depressive patients. These observations suggest a causal relationship: smoking is a self-medication effort to alleviate some symptoms of depression by nicotine. Then, this study investigated nicotine mediatedneurochemical and neuroendocrine alterations in the adaptation response to stress. The modified forced swmming test (FST), a protocol originally employed for screnning new antidepressant drugs, was employed. Male Wistar rats were placed individually into a container (30-cm of water, 24±1ºC, 15 min - pretest). Then animals received nicotine (0.5 mg/kg, s.c.), imipramine (15 mg/kg, i.p.) or saline injections at 1, 19 and 23h after the pretest. One hour after the injections, animals were placed in the same container for 5 min. Immediately after, the animals were sacrificed; dorsal (DH) and ventral (VH) hippocampus, hypothalamus (HT) and dorsal (DR) and median (MR) raphe nuclei were collected by punch for measurement of 5-HT, 5-HIAA and NA by HPLC (expressed in ng/mg tissue). Blood samples were collected for determination of plasma corticosterone levels by radioimmunoassay. The whole hippocampus was also used to evaluate the expression of the 5-HT1A serotoninergic receptor and glucocorticoid receptor by western blot. The effects of prazosin in TNF induced-neurochemical alterations was also evaluated. Nicotine and imipramine decreased in 39% and 50%, respectively, the immobility behavior and increased in 52% and 66%, respectively, the climbing scores, in relation to saline... (Complete abstract click electronic access below)

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Drasdo, Alison L. "Studies of brain nicotinic acetylchlorine receptors : with respect to nicotine dependence." Thesis, University of Bath, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.332792.

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James, John Randolph. "Evidence That Nicotine Can Acutely Desensitize Central Nicotinic Cholinergic Receptors In Vivo." VCU Scholars Compass, 1992. http://scholarscompass.vcu.edu/etd/3935.

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Current concepts concerning nicotine's central nervous system (CNS) mechanism(s) of action suggest that this drug is producing its effects via an interaction at nicotiniccholinergic receptors (nAChRs) which open a membrane cation channel. Following initial opening of the channel, nicotine appears to induce a rapid desensitization of the nAChRs, closing the channel and resulting in a cessation of nicotine's effects. Research presented here will provide evidence of this secondary desensitization process in vivo by demonstrating nicotine's ability to induce acute tolerance in the discriminative stimulus (DS) paradigm. The ability of nicotine to elicit DS control of behavior was significantly reduced via challenge doses of (800, 1200, and 1600 ugjkg, s.c.) of nicotine administered 60-180 minutes prior to the training dose (400 ugjkg, s.c.). Eight out of twenty rats demonstrated this phenomena, with time and dose varying, suggesting that these effect may be contingent upon the individual rat studied. It appears that we have found a means of investigating cellular mechanisms in vivo using operant behavior.

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Jones, Jeb. "Nicotine and responding maintained by conditioned reinforcers effects of two nicotinic antagonists /." [Gainesville, Fla.] : University of Florida, 2009. http://purl.fcla.edu/fcla/etd/UFE0041268.

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Larsen, James D. "Nicotinic Acetylcholine Receptor Dependent Effects of Nicotine on HEK293T and HBO Cells." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5701.

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T2R receptors are the classical bitter taste receptors which detect and transduce bitter taste in a subset of taste receptor cells (TRCs). The TRPM5-dependent T2Rs are G-protein coupled receptors (GPCRs) and are linked to G protein, gustducin to initiate an intracellular signaling cascade for the transduction of bitter tastants. Nicotine is bitter. However, at present the transduction mechanisms for the detection of nicotine in are poorly understood. Previous studies from our laboratory using TRPM5 knockout (KO) mice demonstrated that the T2R pathway is insufficient in explaining the taste perception of nicotine. TRPM5 KO mice elicited chorda tympani (CT) taste nerve responses to nicotine, albeit significantly smaller than the wild type (WT) mice and still responded to nicotine as an aversive stimulus. Following addition of mecamylamine (Mec), a non-specific blocker of neuronal nicotinic acetylcholine receptors (nAChRs), CT responses to nicotine were partially inhibited in both WT and TRPM5 KO mice. Mec also decreases the aversive response to nicotine in both WT and TRPM5 KO mice. These studies led to the hypothesis that both a TRPM5-independent and TRPM5-dependent pathways are responsible for the detection and transduction of the bitter taste of nicotine in TRCs. The TRPM5-independent pathway most likely utilizes the nAChRs expressed in TRCs and function as bitter taste receptors for nicotine. We have subsequently demonstrated the expression of nAChRs in a subset of TRPM5-positive TRCs. However, this mechanism is not well understood in other cell types, particularly undifferentiated epithelial cells, such as HEK293T cells. The specific aims of this project were: (i) To identify which components of T2R-dependent taste reception as well as components of nAChRs are expressed in HEK293T cells; (ii) To determine if HEK293T cells co-express these components; (iii) To identify if exposure to nicotine modulates the expression of T2R and nAChR dependent components in HEK293T cells; (iv) To determine if TRCs express functional nAChR ion channels; and (v) To determine if nAChRs are involved in the release of neuropeptides, such as brain-derived neurotrophic factor (BDNF) in HEK293T cells. The data obtained in HEK293T cells was compared with parallel studies on adult cultured human fungiform taste cells (HBO) done independently by Dr. Jie Qian, a postdoctoral fellow in Dr. Vijay Lyall’s lab. The results of combined studies on HBO and HEK293T cells indicates that TRPM5-positive cells also co-express ionotropic nAChRs, comprising a and β subunits. The nAChRs are capable of forming ion pores and when stimulated by nicotine and create a parallel TRPM5-independent pathway for the detection of nicotine. Using molecular and immunocytochemical techniques, our results demonstrate that mRNAs and proteins for bitter taste receptors and downstream intracellular signaling components as well as subunits necessary for the formation of nAChRs are expressed in HBO and HEK293T cells. Results demonstrated that TRPM5-positive HEK293T cells co-expressed nAChR subunits throughout the entire population. Nicotine increased the influx of Ca2+ in a dose dependent manner, which was somewhat reduced by the addition of TRPM5 blocker, triphenylphosphine oxide (TPPO). Both mRNA and protein expression were altered in a biphasic pattern with a maximum increased observed at 0.5 µM nicotine with a decrease in expression at higher concentrations. The synthesis of neurotrophic factor BDNF, required for maturation of taste bud cells and their innervating nerves, increased in HEK293T cells exposed to nicotine, however, nicotine did not trigger the release of BDNF. These results were then compared and contrasted with HBO cells to better understand the comparative effects of nicotine on both undifferentiated and differentiated cells. The data on HBO cells is presented in the Appendix.

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DiMaggio, Stassi. "Development of Novel Nicotinic Receptor Mediated Therapeutic Agents: Synthesis and Biological Evaluation of Novel Epibatidine Analogs and the First Total Synthesis of Anabasamine and Related Analogs." ScholarWorks@UNO, 2003. http://scholarworks.uno.edu/td/40.

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In an effort to search for a more selective, less toxic neuronal nicotinic acetylcholine receptor analgesic agent in comparison to epibatidine, a series of analogs with hybrid structures of epibatidine and ABT-594 were designed and synthesized. The 1-(pyridyloxymethyl)-7-azabicyclo[2.2.1]heptane ring systems were furnished via an intramolecular cyclization from a trans 1, 4 disubstitituted amino-cyclohexane derivative. The functionalized cyclohexane ring was formed via a [4+2] Diels-Alder cyclization reaction between the acetamidoacrylate and Danishefsky's diene. These 1- (pyridyloxymethyl)-7-azabicyclo[2.2.1]heptane ring systems were then tested in vitro as potential á4â2 nicotinic acetylcholine receptor ligands with high potency and selectivity. In addition, a series of rigid acetylcholine analogs were synthesized from cocaine to study the conformation of acetylcholine, the endogenous neurotransmitter at the nicotinic acetylcholine receptor. A stereoselective reduction of 2-tropinone led to the enantioselective synthesis of the desired acetoxytropane systems. These compounds were also tested in in vivo models for binding affinity and efficacy responses. Anabasamine, an alkaloid isolated from the Central Asian shrub, Anabasis aphylla, was synthesized for the first time. It was targeted due to interesting preliminary biological activity such as exhibiting anticholinesterase activity, anti-inflammatory activity, and facilitated an increase in hepatic alcohol dehydrogenase levels. Only preliminary studies were performed as anabasamine is limited in quantity due to its difficult isolation. A versatile synthetic methodology was developed for the synthesis of anabasamine and related nicotine analogs. This new methodology employed a pyridyl anion addition to valerolactone, for anabasamine, or butyrolactone for the nicotine analog, to afford 5-hydroxy-1-(6-methoxy-pyridin-3-yl)-pentan-1-one or 4-hydroxy-1-(6- methoxy-pyridin-3-yl)-butan-1-one, respectively. A reductive amination provided the piperidine ring moiety and a Suzuki coupling reaction introduced the bipyridyl moiety to anabasamine in five steps and 23% overall yield. In addition, this methodology was applied successfully to the synthesis of nicotine and other related analogs. In particular the synthesis of 6-methoxynicotine, a useful drug intermediate, was generated improving the yield from 16% over five steps to 54% over three steps.

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Bowker, Katharine. "The effectiveness of nicotine replacement therapy during pregnancy : investigating the role of nicotine substitution, nicotine metabolism and pregnant smokers' experiences." Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/32138/.

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Nicotine replacement therapy (NRT) is effective in non-pregnant populations at assisting smoking cessation, but there is no evidence that NRT can help pregnant smokers to stop. Nicotine metabolism increases during pregnancy, and so the nicotine dose delivered by NRT could be insufficient for ameliorating withdrawal symptoms. However, little is known about the level of nicotine substitution provided by NRT or the pattern of nicotine metabolism during pregnancy. Also low adherence to NRT may explain why NRT does not appear to be effective. The overall aim of this thesis was to increase understanding as to why NRT does not appear to be effective during pregnancy. The thesis consists of three studies. The first study involved analysing data on 33 pregnant participants from the NRT arm of a randomised control trial who had stopped smoking and were still using 15mg/16hr nicotine patches 1 month after quitting. Salivary cotinine levels when smoking at baseline were compared with levels on NRT at 1 month. Cotinine levels were lower than those achieved from smoking (median 98.5ng/ml while smoking and 62.8ng/ml while using NRT and remaining abstinent, p = 0.045). The second study involved 101 pregnant smokers, who were asked to provide saliva samples to measure NMR at 8-14 weeks, 18-22 weeks , 32-36 weeks gestation, 4 weeks postpartum and 12 weeks postpartum . Compared with NMR at 12 weeks postpartum, NMR was significantly higher at 18-22 weeks (26% higher, 95% CI 12% to 38%) and 32-36 weeks (23% higher, 95% CI 9% to 35%). There was no difference between the 8-14 weeks gestation or 4 weeks postpartum NMR and 12 weeks postpartum. The third study was a qualitative study that involved semi-structured telephone interviews with 14 pregnant smokers who had recently been prescribed NRT, but self-reported low NRT adherence or discontinuing treatment prematurely. Thematic analysis was used to analyse data. Most smoked regularly while using NRT and many used NRT to cut down their cigarette intake rather than to quit abruptly. Some were concerned that using NRT instead of smoking could actually increase their nicotine dependency or cause greater harm to the fetus, and consequently often underutilised NRT. This thesis supports the hypothesis that NRT at standard doses may be ineffective in pregnancy due to increased metabolism. The effectiveness of NRT may be hindered by the way in which NRT is used in pregnancy.

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Vallaster, Markus Parzival. "Intergenerational Effects of Nicotine in an Animal Model of Paternal Nicotine Exposure." eScholarship@UMMS, 2017. https://escholarship.umassmed.edu/gsbs_diss/913.

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Environmental conditions imposed onto organisms during certain phases of their life cycles such as embryogenesis or puberty can not only impact the organisms’ own health, but also affect subsequent generations. The underlying mechanisms causing intergenerational phenotypes are not encoded in the genome, but the result of reversible epigenetic modifications. This work investigates in a mouse model the impact of paternal nicotine exposure on the next generation regarding addictive behavior modulation, metabolic changes, and molecular mechanisms. It provides evidence that male offspring from nicotine-exposed fathers (NIC offspring) is more resistant to lethal doses of nicotine. This phenotype is gender-specific and depends on short-term environmental challenges with low doses of nicotine prior to the LD50 application. The observed survival phenotype is not restricted to nicotine as drug of abuse, but also presents itself, when NIC offspring is challenged with a cocaine LD50 after acclimatization to low doses of either nicotine or cocaine. Functionally, NIC offspring metabolizes nicotine faster than control. Mechanistically, NIC offspring livers show global up-regulation of xenobiotic processing genes (XPG), an effect that is even more pronounced in primary hepatocyte cultures. Being known targets of Constitutive Androstane Receptor (CAR) and Pregnane X Receptor (PXR), these XPGs show higher baseline expression in naïve NIC offspring livers. Nicotine’s action on the brain’s reward circuitry does not appear to be of biological significance in our model system. Taken together, paternal nicotine exposure leads to a non-specific and conditional phenotype in male NIC offspring that may provide a general survival advantage against xenobiotic challenges.

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Vallaster, Markus Parzival. "Intergenerational Effects of Nicotine in an Animal Model of Paternal Nicotine Exposure." eScholarship@UMMS, 2008. http://escholarship.umassmed.edu/gsbs_diss/913.

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Books on the topic "Nicotine"

Price, Sean. Nicotine. New York: Chelsea House, 2008.

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Wagner, Heather Lehr. Nicotine. Edited by Triggle D. J. Philadelphia: Chelsea House Publishers, 2003.

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Henningfield, Jack E., Edythe D. London, and Sakire Pogun, eds. Nicotine Psychopharmacology. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-69248-5.

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National Institute on Drug Abuse, ed. Nicotine addiction. [Washington, D.C.]: National Institute on Drug Abuse, U.S. Dept. of Health and Human Services, National Institutes of Health, 1998.

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DeAngelis, Gina. Nicotine & cigarettes. Philadelphia: Chelsea House Publishers, 2000.

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Hofmann, F. B. Nicotine Psychopharmacology. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009.

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National Institute on Drug Abuse., ed. Nicotine addiction. [Washington, D.C.]: National Institute on Drug Abuse, U.S. Dept. of Health and Human Services, National Institutes of Health, 1998.

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Yann. Nicotine goudron. Paris: L'Echo des savanes, 1990.

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National Institute on Drug Abuse., ed. Nicotine addiction. [Washington, D.C.]: National Institute on Drug Abuse, U.S. Dept. of Health and Human Services, National Institutes of Health, 1998.

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Hasan, Heather. Caffeine and nicotine. New York: Rosen Pub., 2009.

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Book chapters on the topic "Nicotine"

Andrews, Anne M., Greg A. Gerhardt, Lynette C. Daws, Mohammed Shoaib, Barbara J. Mason, Charles J. Heyser, Luis De Lecea, et al. "Nicotine." In Encyclopedia of Psychopharmacology, 877–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_303.

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Davies, Marilyn. "Nicotine." In Encyclopedia of Women’s Health, 892–94. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-0-306-48113-0_298.

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Sershen, Henry. "Nicotine." In Alterations of Metabolites in the Nervous System, 263–78. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4757-6740-7_10.

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Nakajima, Motohiro, and Mustafa al’Absi. "Nicotine." In Encyclopedia of Behavioral Medicine, 1502–3. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_268.

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Tiro, Jasmin, Simon J. Craddock Lee, Steven E. Lipshultz, Tracie L. Miller, James D. Wilkinson, Miriam A. Mestre, Barbara Resnick, et al. "Nicotine." In Encyclopedia of Behavioral Medicine, 1334–35. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_268.

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Clarke, Paul B. S. "Nicotine." In Encyclopedia of Psychopharmacology, 1100–1107. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-36172-2_303.

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Henningfield, J. E., R. M. Keenan, and P. B. S. Clarke. "Nicotine." In Pharmacological Aspects of Drug Dependence, 271–314. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-60963-3_8.

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Hsia, Stephanie L., Anna K. Mischel, and Arthur L. Brody. "Nicotine." In Absolute Addiction Psychiatry Review, 105–20. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-33404-8_7.

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Milhorn, H. Thomas. "Nicotine." In Drug and Alcohol Abuse, 285–93. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4899-6126-6_24.

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George, David J. "Nicotine." In Poisons, 97–103. Boca Raton : CRC Press, [2018]: CRC Press, 2017. http://dx.doi.org/10.1201/9781315371757-13.

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Conference papers on the topic "Nicotine"

Campanella, L., R. Cocco, G. Favero, M. P. Sammartino, and M. Tomassetti. "INHIBITION ENZYME SENSOR FOR NICOTINE, NICOTINAMIDE AND NICOTINIC ACID DETERMINATION." In Proceedings of the 5th Italian Conference — Extended to Mediterranean Countries. WORLD SCIENTIFIC, 2000. http://dx.doi.org/10.1142/9789812792013_0005.

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Smith, Danielle, Lynn Kozlowski, Richard O'Connor, Andrew Hyland, Maciej Goniewicz, and Lorraine Collins. "Reasons for individual and concurrent use of vaped nicotine and cannabis: their similarities, differences, and association with product use." In 2021 Virtual Scientific Meeting of the Research Society on Marijuana. Research Society on Marijuana, 2022. http://dx.doi.org/10.26828/cannabis.2022.01.000.15.

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Background: Understanding similarities, differences, and associations between reasons people use vaped nicotine and cannabis may be important for identifying underlying contributors to co-use. Methods: A cross-sectional survey of n=112 co-users of vaped nicotine and cannabis was conducted in 2020. Participants reported on their use of nicotine and cannabis products (vaped and smoked), along with reasons for individual product use, nicotine-cannabis co-use, and engagement with sequential use and co-administration. Results: Cannabis vaping and smoking exhibited similar ratings for user experience and product/substance-related reasons for use. Reasons related to product utility were similar for cannabis vaping and nicotine vaping. Ratings for utility-related reasons for use were significantly higher for cannabis vaping than cannabis smoking (mean (SD):3.6(±1.0) vs. 2.6(±1.2), difference=0.98, t=7.84, p<0.0001). Harm reduction-related reasons for use were rated higher for nicotine vaping than cannabis vaping (2.4(±1.6) vs. 1.8(±1.4), difference=0.65, t=4.24, p<0.0001). Regression models showed higher ratings for utility-related and harm reduction-related reasons for nicotine vaping were significantly associated with more frequent nicotine vaping (both p<0.05). Greater endorsement of instrumentality-related reasons for co-use corresponded with more frequent monthly nicotine vaping and a three-fold increase in odds of ever chasing cannabis with nicotine. Conclusions: Vaping serves purposes that differ by substance; nicotine vaping was more closely related to reducing tobacco smoking-related harms, and cannabis vaping was more closely related to circumventing social problems posed by cannabis smoking. Lifetime sequential co-use practices and more frequent nicotine vaping were associated with enhancing the intoxicating effects of cannabis. Findings have implications for understanding nicotine and cannabis co-use.

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Hans, Hesketh, Mila Citrawati, and Citra Ayu Aprilia. "The Effect of Electric Cigarette Nicotine Levels on Peak Expiratory Flow in Vape User Communities, South Jakarta." In The 7th International Conference on Public Health 2020. Masters Program in Public Health, Universitas Sebelas Maret, 2020. http://dx.doi.org/10.26911/the7thicph.02.14.

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Background: Electronic Cigarette is one form of many nicotine replacement therapy (NRT) that uses energy from battery to deliver nicotine in gas form and by World Health Organization (WHO) defined as Electronic Nicotine Delivery System (ENDS). This study aimed to investigated the effect of electronic cigarette’s nicotine dosage on the peak expiratory flow (PEF). Subjects and Method: This was a cross sectional study conducted at VH Community-South Jakarta from February to march 2018. A Sample of 72 vapers was selected by consecutive sampling. It was divided into 3 groups: vapers who used 3 mg, 6 mg, and 12 mg nicotine dosage. The inclusion criteria were electric smokers healthy participants aged 19-24 years, normal body mass index, moderate physical activity, and only used e-cigarettes for more than 12 months. The exclusion criteria were the respondent had a history of respiratory disease. The dependent variable was peak expiratory flow (PEF). The independent variable was the nicotine dosage which obtained in electronic cigarette’s liquid. The research instrument used by Peak Flow Meter (PFM). The data was analyzed by Chi-square. Results: Chi-Square analysis showed the effect of electronic cigarette’s nicotine dosages to PEF (OR= 7.2; p< 0.001). Conclusion: The result showed that nicotine dosage which obtained in electronic cigarette’s liquid had effects with PEF. Therefore, each nicotine dosage has different effects to respiratory health. Because nicotine increases endothelial permeability, inhibits cell endothelial proliferation, and caused goblet cell metaplasia. Keyword: Electronic Cigarette, Nicotine, Peak Expiratory Flow Correspondence: Mila Citrawati. Departemen Fisiologi, FK UPN “Veteran” Jakarta. Jl. RS Fatmawati, Pondok Labu, South Jakarta 12450. E-mail: milacitrawati@upnvj.ac.id. Mobile: (021) 7656971. DOI: https://doi.org/10.26911/the7thicph.02.14

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BOUTHERIN-FALSON, O., and N. BLAES. "EFFECT OF NICOTINE ON HUMAN UMBILICAL VEIN ENDOTHELIAL CELLS IN CULTURE : PROSTACYCLIN PRODUCTION AND PROLIFERATION STUDIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643378.

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Clinical observations and results from animal studies indicate that nicotine may play a role in vascular disorders related to smoking. It has been reported that nicotine could alter vascular prostacyclin (PGI2) production and increase the number of circulating endothelial cells. In the present study, the direct effect of nicotine on endothelial cells in culture was investigated : Both PGI2 production and proliferative abilities were studied.PGI2 production studies : human umbilical vein endothelial cells (HUVEC) were grown in 4 days to confluency in control medium (RPM/199 1:1 + 20% fetal calf serum). At the beginning of the experiments, medium was replaced by tyrode Hepes buffer added or not with nicotine at different concentrations (0.05,0.5, 5, 50 or 200 ug/ml). Basal production of PGI2, assessed after 20 minutes, was significantly increased by 0.5 ug/ml nicotine (223% of control) ; subsequently thrombin (1 U/ml) stimulated release was measured after 5 minutes, it was dose dependently decreased by nicotine. Thus, at least in basal conditions, nicotine treatment of HUVEC alone in culture did not permit us to reproduce the inhibitory effects described on models involving smooth muscle cells in addition to the endothelial cells. Otherwise, nicotine could interfere with stimulating agents such as thrombin. Investigations on the effect of these agents in combination are currently in progressProliferation studies : Cells were grown in nicotine or control medium. Proliferation ability, estimated by the increase in cell number at daily interval was slighly increased in cultures receiving 0.05 ug/ml nicotine (110.4% of control). This tendancy was confirmed by 3H Thymidine incorporation (+41%). On the contrary a decrease in cell density was observed for the highest concentrations, from 50 ug/ml. This later effect did not seem to be related to any cytotoxicity or cell detachment. Thus, endothelial cells appeared to be highly responsive to nicotine in their PGI2 production while their growth characteristics were rather resistant to nicotine treatment.

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Fitzke, Reagan, Jordan Davis, and Eric Pedersen. "Co-use of Tobacco/Nicotine and Cannabis Among Veterans: A Preliminary Investigation of Prevalence and Associations with Mental Health Outcomes." In 2020 Virtual Scientific Meeting of the Research Society on Marijuana. Research Society on Marijuana, 2021. http://dx.doi.org/10.26828/cannabis.2021.01.000.10.

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While tobacco and cannabis use rates remain high in the general U.S. population, veterans from the conflicts in Iraq and Afghanistan (i.e., OEF/OIF veterans) are at particularly high risk of high rates of cannabis and tobacco use. Co-use of tobacco/nicotine and cannabis (i.e., using both substances within a specified period of time or combining the drugs within the same device for use) is of growing prevalence in the United States. Tobacco/nicotine and cannabis use is often associated with poor mental health outcomes such as stress, anxiety, and depression. However, little is understood about the prevalence rates of tobacco/nicotine and cannabis co-use among U.S. veterans as well as associations with mental health symptomology. The current study aimed to investigate types of tobacco/nicotine and cannabis co-use among veterans, as well as associations between co-use and mental health outcomes of stress, depression, anxiety, and posttraumatic stress disorder. Participants (N= 1,548) were recruited through social media websites and completed an online survey as part of a larger study. The majority (80%) endorsed tobacco/nicotine and/or cannabis use in the past 30 days. Descriptive analyses were run to assess prevalence of use within the sample. Mean comparisons were conducted to assess differences in past 30-day frequency of use and for mental health outcomes between co-users and single users of either substance. Among the larger sample, 90% endorsed lifetime use of tobacco/nicotine, 23% endorsed lifetime use of cannabis, and 21% endorsed any lifetime co-use of both substances. These participants also endorsed past 30 day use of tobacco/nicotine (77%), cannabis (10%), and co-use (7%). Among the past 30-day cannabis users, 66% reported also using tobacco/nicotine, while 9% of past 30-day tobacco/nicotine users also reported cannabis use. When comparing cannabis-only users to co-users of cannabis and tobacco/nicotine, anxiety symptoms were reported as significantly higher among co-users. Tobacco/nicotine-only users endorsed higher past 30-day frequency of cigarettes and e-cigarettes compared to co-users; however, co-users endorsed significantly higher levels of stress and symptoms of PTSD, depression, and anxiety compared to tobacco/nicotine-only users. Results suggest that the addition of cannabis use in conjunction with tobacco/nicotine use may be associated with greater mental health symptoms among veterans. Findings have implications for future veteran mental health care and substance use treatment among tobacco/nicotine and cannabis co-users.

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Nenadović, Milena, Katja Kržišnik, Polonca Trebše, and Mojca Bavcon Kralj. "Effect of Time, pH, Alcohol and Sugar Content on Nicotine Re-lease from Pouches Available on Slovene Market." In Socratic lectures 10. University of Lubljana Press, 2024. http://dx.doi.org/10.55295/psl.2024.ii7.

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Abstract: Tobacco-free nicotine pouches, first introduced in Sweden, are made as a less hazardous product for cigarette consumers. Instead of tobacco leaves, they consist of nicotine-containing powder and other ingredients such as water, salts, natural aromatic oils and others, that will boost the flavor and effect and make it last longer. This research aimed to investigate the extraction efficiency of nicotine from poaches of different brands. The effects of alcohol and sugars present in saliva at different pHs and consumption times were investigated as well. We optimized a High performance liquid chromatography with diode-array detection method (HPLC-DAD) for nicotine determination and its quantification. We used reversed-phase chromatography (RP-HPLC), and a mixture of sodium hydrogen carbonate and acetonitrile as a mobile phase (85:15, v/v). Different brands of nicotine pouches were used. Nicotine extraction rate showed positive linear dependence on time. The percentage of extraction was measured at different intervals, up to two hours, without getting a plateau. Nicotine extraction lowers with the increasing volume of saliva. The obtained results have shown that the increasing ethanol concentration in saliva (from 5-40 %) leads to a higher extraction rate, coming up to 85 %. In the case of sugar addition, the results were variable. Experiments with White fox pouches have shown that extraction of nicotine decreases with a higher concentration. On contrary, Siberia pouches do not exhibit that correlation. When it comes to pH, we used pH range that usually varies in saliva and the results have shown no significant differences. Keywords: Nicotine, Pouches, HPLC-DAD, Extraction

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Zobena, Aija. "Student Tobacco Use Behaviours: A Qualitative Study of Alternative Tobacco and Nicotine Product Use in Young Adulthood." In 14th International Scientific Conference "Rural Environment. Education. Personality. (REEP)". Latvia University of Life Sciences and Technologies. Faculty of Engineering. Institute of Education and Home Economics, 2021. http://dx.doi.org/10.22616/reep.2021.14.043.

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Non-combustible alternative tobacco products such as tobacco-free nicotine pouches, heated tobacco, and electronic cigarettes (e-cigarettes) marketed as less harmful alternatives to cigarettes as smoking cessation aids are becoming increasingly popular among adolescents and young adults. This age group includes individuals still experimenting with and establishing tobacco use. The aim of the study is to investigate student tobacco use behaviours, particularly novel devices, and alternative products to understand how to decrease tobacco initiation and use among adolescents and young adults. In August 2020, two focus group discussions were organized to obtain information on young people's experience of alternative tobacco and nicotine product use. In each of them, high school students (aged over 18) and students took part. The participants of the focus group discussion were chosen by the “snowball” method. Cessation of smoking and replacing cigarettes with alternative tobacco and nicotine products reduce some of the harmful effects but are not harmless and nicotine addiction remains. By replacing cigarette smoking with the use of tobacco-free nicotine pouches, heated tobacco, or e-cigarettes, one form of nicotine use is being replaced by another. According to the study, young people have no understanding of nicotine addiction and the health risks of using alternative tobacco products. Today's adolescents and young adults often see consumption of tobacco and nicotine products as a mean to construct and project their unique identity.

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Fathi, Raden Muhammad, Ahmad Fauzantoro, Siti Fauziyah Rahman, and Misri Gozan. "Column chromatography isolation of nicotine from tobacco leaf extract (Nicotiana tabaccum L.)." In 2ND BIOMEDICAL ENGINEERING’S RECENT PROGRESS IN BIOMATERIALS, DRUGS DEVELOPMENT, AND MEDICAL DEVICES: Proceedings of the International Symposium of Biomedical Engineering (ISBE) 2017. Author(s), 2018. http://dx.doi.org/10.1063/1.5023958.

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Esther, C. R., W. K. O'Neal, A. L. Koch, C. B. Cooper, I. Barjaktarevic, L. Raffield, R. P. Bowler, et al. "Prolonged, Physiologically Relevant Concentrations of Nicotine and Nicotine Metabolites in Airways of Smokers." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1907.

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Girdhar, Gaurav, Sulan Xu, Jolyon Jesty, and Danny Bluestein. "E-Selectin Expression on Endothelial Cells in the Presence of Platelets and Cigarette Smoke Extract." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192154.

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Cigarette smoking is a risk factor for development of cardiovascular (CV) disease [1], with increased platelet activation due to cigarette smoke involving a major part of this risk.[2] We have shown that this smoke-induced platelet activation is largely due to the non-nicotine smoke components and their effects can be effectively modulated in the presence of nicotine.[3] However, the effects of nicotine and non-nicotine cigarette smoke components need to be confirmed more physiologically in the presence of endothelial cells (ECs). Prior in-vitro studies have shown that high concentrations of cigarette smoke extract (CSE) increase adhesion molecule expression on ECs.[4] These studies however preclude the involvement of physiological shear stresses and are performed on ECs alone. To overcome these limitations and investigate ECs-platelets together in one system under shear stress, we use a hemodynamic shear device (HSD) that combines features of the cone and plate, and the annular Couette viscometer (to facilitate platelet sampling). We test the following hypotheses — (1) smoke-activated platelets and the nicotine-free extract would confer a synergistic E-selectin expression on ECs, and (2) in contrast to conventional cigarette extracts, nicotine-free smoke extracts would increase platelet activation more significantly, and that this effect may be independent of the presence of ECs.

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Reports on the topic "Nicotine"

Lillard, Dean. The Economics of Nicotine Consumption. Cambridge, MA: National Bureau of Economic Research, March 2020. http://dx.doi.org/10.3386/w26912.

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Tauras, John, and Frank Chaloupka. The Demand for Nicotine Replacement Therapies. Cambridge, MA: National Bureau of Economic Research, June 2001. http://dx.doi.org/10.3386/w8332.

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Guillaumier, A., K. McCarter, J. Trigg, S. Hines, M. Jackson, N. Harrison, S. Ishaque, et al. Managing nicotine dependence in clinical settings. The Sax Institute, June 2023. http://dx.doi.org/10.57022/zuzh3201.

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Abstract:

This Evidence Check aims to identify the most effective clinical interventions for nicotine-dependent patients in clinical settings. The Evidence Check identified 74 eligible studies for inclusion in the review, and the National Health and Medical Research Council (NHMRC) Levels of Evidence were used to assess the robustness of the included studies. According to the evidence, a multi-component approach involving both medications and behavioural interventions remains the best practice for quitting smoking and is recommended to support quitting smoking for nicotine-dependent patients. The medicine Varenicline continues to be the most effective stand-alone treatment. The evidence suggests that for patients who can't take varenicline, Nicotine Replacement Therapy plus behavioural support should be provided. During hospital stays, healthcare providers should provide a connection to Quitline alongside behavioural interventions and medicines. The same advice should be followed for e-cigarette cessation since there is a lack of evidence assessing quitting strategies specific to e-cigarette use.

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Carlezon, Jr, and William A. Nicotine Effects on the Impact of Stress. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada612315.

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Carlezon, Jr, and William A. Nicotine effects on the impact of stress. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada591378.

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Carlezon, Jr, and William A. Nicotine Effects on the Impact of Stress. Fort Belvoir, VA: Defense Technical Information Center, September 2015. http://dx.doi.org/10.21236/ada624296.

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Roman, Jesse. Prenatal Exposure to Nicotine and Childhood Asthma: Role of Nicotine Acetylcholine Receptors, Neuropeptides, and Fibronectin Expression in Lung. Fort Belvoir, VA: Defense Technical Information Center, December 2005. http://dx.doi.org/10.21236/ada452269.

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Roman, Jesse. Prenatal Exposure to Nicotine and Childhood Asthma: Role of Nicotine Acetylcholine Receptors, Neuropeptides and Fibronectin Expression in Lung. Fort Belvoir, VA: Defense Technical Information Center, December 2008. http://dx.doi.org/10.21236/ada508588.

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Apatov, Nathaniel M. Nicotine-Induced Antinociception in Male and Female Sprague-Dawley Rats. Fort Belvoir, VA: Defense Technical Information Center, June 1999. http://dx.doi.org/10.21236/ad1012097.

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Saffer, Henry, Melanie Wakefield, and Yvonne Terry-McElrath. The Effect of Nicotine Replacement Therapy Advertising on Youth Smoking. Cambridge, MA: National Bureau of Economic Research, March 2007. http://dx.doi.org/10.3386/w12964.

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Academic literature on the topic 'Nicotine'

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Contents

Journal articles on the topic "Nicotine"

Dissertations / Theses on the topic "Nicotine"

Books on the topic "Nicotine"

Book chapters on the topic "Nicotine"

Conference papers on the topic "Nicotine"

Reports on the topic "Nicotine"