path(MESH:"Tobacco Use Disorder")
Recent studies have supported a role for ERK and CREB activity in neural plasticity associated with nicotine addiction (71, 381, 484). It has also been proposed that the ERK and JAK-2/STAT-3 signaling pathways contribute to the toxic effects of nicotine in skin cells (42), and other pathways contribute to the effects of nicotine and other nicotinic ligands on inflammatory responses as described below. PubMed:19126755
Recent studies have supported a role for ERK and CREB activity in neural plasticity associated with nicotine addiction (71, 381, 484). It has also been proposed that the ERK and JAK-2/STAT-3 signaling pathways contribute to the toxic effects of nicotine in skin cells (42), and other pathways contribute to the effects of nicotine and other nicotinic ligands on inflammatory responses as described below. PubMed:19126755
It has long been known that smokers tend to be leaner, and yet approximately four times more likely to become insulin resistant and develop type I diabetes (497), a condition that is more commonly observed in obese patients. PubMed:19126755
However, epidemiological studies have reported that heavy smokers are less likely to experience PD (see reviews in Refs. 384, 385). PubMed:19126755
In fact, the relationship between tobacco abuse (including smokeless) and difficulty in healing, increased susceptibility to infection (especially oral), enhanced expression of indicators of skin aging, and increased cancer risk are all well-documented (383, 452). PubMed:19126755
In fact, the relationship between tobacco abuse (including smokeless) and difficulty in healing, increased susceptibility to infection (especially oral), enhanced expression of indicators of skin aging, and increased cancer risk are all well-documented (383, 452). PubMed:19126755
In fact, the relationship between tobacco abuse (including smokeless) and difficulty in healing, increased susceptibility to infection (especially oral), enhanced expression of indicators of skin aging, and increased cancer risk are all well-documented (383, 452). PubMed:19126755
Indeed, presynaptic effects of nAChRs in regulating dopamine release in basal ganglia and prefrontal cortex likely participate in nicotine’s addictive and cognitive effects, respectively (Jasinska et al., 2014) PubMed:28445721
Developmental changes in nAChR functions may play a role in nicotine addiction, as a central question in tobacco control is young adult smokers’ marked sensitivity to developing nicotine dependence (DSM-V Nicotine Workgroup, 2010; DiFranza et al., 2000; Difranza, 2010) PubMed:21482353
Single-nucleotide polymorphisms found in the human alpha5, alpha3, beta4 gene cluster are associated with nicotine dependence and its age-dependent onset; number of cigarettes smoked per day and ‘‘pleasurable buzz’’ elicited by smoking; alcoholism, sensitivity to the depressant effects of alcohol, and age of alcohol initiation; cocaine dependence; opioid dependence; lung cancer; and cognitive flexibility (Erlich et al., 2010; Hansen et al., 2010; Improgo et al., 2010; Saccone et al., 2010; Zhang et al., 2010) PubMed:21482353
Mutations in nicotinic receptor subunits are linked to human disease, alpha4 and beta2 in some epilepsies, alpha7 in schizophrenia, and alpha5 in nicotine addiction; and each mutation ultimately manifests itself as an imbalance in the properties of neuronal circuits PubMed:21482353
Single-nucleotide polymorphisms found in the human alpha5, alpha3, beta4 gene cluster are associated with nicotine dependence and its age-dependent onset; number of cigarettes smoked per day and ‘‘pleasurable buzz’’ elicited by smoking; alcoholism, sensitivity to the depressant effects of alcohol, and age of alcohol initiation; cocaine dependence; opioid dependence; lung cancer; and cognitive flexibility (Erlich et al., 2010; Hansen et al., 2010; Improgo et al., 2010; Saccone et al., 2010; Zhang et al., 2010) PubMed:21482353
Single-nucleotide polymorphisms found in the human alpha5, alpha3, beta4 gene cluster are associated with nicotine dependence and its age-dependent onset; number of cigarettes smoked per day and ‘‘pleasurable buzz’’ elicited by smoking; alcoholism, sensitivity to the depressant effects of alcohol, and age of alcohol initiation; cocaine dependence; opioid dependence; lung cancer; and cognitive flexibility (Erlich et al., 2010; Hansen et al., 2010; Improgo et al., 2010; Saccone et al., 2010; Zhang et al., 2010) PubMed:21482353
Third, persons with schizophrenia have the greatest rate and intensity of cigarette smoking of any identifiable subgroup in the population PubMed:21482353
b4 subunit mRNA colocalizes with a4 subunit mRNA in many brain regions [37,38] that could be involved in complex behaviors including nicotine dependence. PubMed:21787755
This makes the hypothesis particularly intriguing that a6*-nAChRs play roles in nicotine dependence. PubMed:21787755
a4b2-nAChRs have been implicated in nicotine self-administration, reward, and depen- dence, and in diseases such as Alzheimer’s and epilepsy [1–5,27–33]. PubMed:21787755
Human genetic studies have shown that the non- synonymous coding SNP D398N is associated with lung cancer and nicotine dependence PubMed:28901280
Recent studies have supported a role for ERK and CREB activity in neural plasticity associated with nicotine addiction (71, 381, 484). It has also been proposed that the ERK and JAK-2/STAT-3 signaling pathways contribute to the toxic effects of nicotine in skin cells (42), and other pathways contribute to the effects of nicotine and other nicotinic ligands on inflammatory responses as described below. PubMed:19126755
Recent studies have supported a role for ERK and CREB activity in neural plasticity associated with nicotine addiction (71, 381, 484). It has also been proposed that the ERK and JAK-2/STAT-3 signaling pathways contribute to the toxic effects of nicotine in skin cells (42), and other pathways contribute to the effects of nicotine and other nicotinic ligands on inflammatory responses as described below. PubMed:19126755
In fact, the relationship between tobacco abuse (including smokeless) and difficulty in healing, increased susceptibility to infection (especially oral), enhanced expression of indicators of skin aging, and increased cancer risk are all well-documented (383, 452). PubMed:19126755
There is current evidence that nAChRs present in skin cells modulate the responses triggered by inflammatory stimuli applied to the skin (354). Smoking is a welldefined risk factor in delayed wound healing and possibly the development of premature facial wrinkling (226). PubMed:19126755
In fact, the relationship between tobacco abuse (including smokeless) and difficulty in healing, increased susceptibility to infection (especially oral), enhanced expression of indicators of skin aging, and increased cancer risk are all well-documented (383, 452). PubMed:19126755
In fact, the relationship between tobacco abuse (including smokeless) and difficulty in healing, increased susceptibility to infection (especially oral), enhanced expression of indicators of skin aging, and increased cancer risk are all well-documented (383, 452). PubMed:19126755
There is current evidence that nAChRs present in skin cells modulate the responses triggered by inflammatory stimuli applied to the skin (354). Smoking is a welldefined risk factor in delayed wound healing and possibly the development of premature facial wrinkling (226). PubMed:19126755
In fact, the relationship between tobacco abuse (including smokeless) and difficulty in healing, increased susceptibility to infection (especially oral), enhanced expression of indicators of skin aging, and increased cancer risk are all well-documented (383, 452). PubMed:19126755
Modulation by nicotine of inflammatory responses in the intestines is much better reported. Early studies found that patients with ulcerative colitis who stopped smoking tobacco developed the disease or exhibited more severe disease progression, which was ameliorated by either returning to smoking (58, 401, 466), or, in some cases, administering nicotine through transdermal patches (313).In contrast, patients with Crohn’s disease experience much more severe disease when smoking (401). PubMed:19126755
Modulation by nicotine of inflammatory responses in the intestines is much better reported. Early studies found that patients with ulcerative colitis who stopped smoking tobacco developed the disease or exhibited more severe disease progression, which was ameliorated by either returning to smoking (58, 401, 466), or, in some cases, administering nicotine through transdermal patches (313).In contrast, patients with Crohn’s disease experience much more severe disease when smoking (401). PubMed:19126755
It has long been known that smokers tend to be leaner, and yet approximately four times more likely to become insulin resistant and develop type I diabetes (497), a condition that is more commonly observed in obese patients. PubMed:19126755
However, epidemiological studies have reported that heavy smokers are less likely to experience PD (see reviews in Refs. 384, 385). PubMed:19126755
Indeed, presynaptic effects of nAChRs in regulating dopamine release in basal ganglia and prefrontal cortex likely participate in nicotine’s addictive and cognitive effects, respectively (Jasinska et al., 2014) PubMed:28445721
Mutations in nicotinic receptor subunits are linked to human disease, alpha4 and beta2 in some epilepsies, alpha7 in schizophrenia, and alpha5 in nicotine addiction; and each mutation ultimately manifests itself as an imbalance in the properties of neuronal circuits PubMed:21482353
Single-nucleotide polymorphisms found in the human alpha5, alpha3, beta4 gene cluster are associated with nicotine dependence and its age-dependent onset; number of cigarettes smoked per day and ‘‘pleasurable buzz’’ elicited by smoking; alcoholism, sensitivity to the depressant effects of alcohol, and age of alcohol initiation; cocaine dependence; opioid dependence; lung cancer; and cognitive flexibility (Erlich et al., 2010; Hansen et al., 2010; Improgo et al., 2010; Saccone et al., 2010; Zhang et al., 2010) PubMed:21482353
Developmental changes in nAChR functions may play a role in nicotine addiction, as a central question in tobacco control is young adult smokers’ marked sensitivity to developing nicotine dependence (DSM-V Nicotine Workgroup, 2010; DiFranza et al., 2000; Difranza, 2010) PubMed:21482353
Third, persons with schizophrenia have the greatest rate and intensity of cigarette smoking of any identifiable subgroup in the population PubMed:21482353
Single-nucleotide polymorphisms found in the human alpha5, alpha3, beta4 gene cluster are associated with nicotine dependence and its age-dependent onset; number of cigarettes smoked per day and ‘‘pleasurable buzz’’ elicited by smoking; alcoholism, sensitivity to the depressant effects of alcohol, and age of alcohol initiation; cocaine dependence; opioid dependence; lung cancer; and cognitive flexibility (Erlich et al., 2010; Hansen et al., 2010; Improgo et al., 2010; Saccone et al., 2010; Zhang et al., 2010) PubMed:21482353
Single-nucleotide polymorphisms found in the human alpha5, alpha3, beta4 gene cluster are associated with nicotine dependence and its age-dependent onset; number of cigarettes smoked per day and ‘‘pleasurable buzz’’ elicited by smoking; alcoholism, sensitivity to the depressant effects of alcohol, and age of alcohol initiation; cocaine dependence; opioid dependence; lung cancer; and cognitive flexibility (Erlich et al., 2010; Hansen et al., 2010; Improgo et al., 2010; Saccone et al., 2010; Zhang et al., 2010) PubMed:21482353
Because alpha4beta2 nAChRs are the most susceptible to nicotine-induced upregulation, the data again seem consistent with the idea that selective upregulation of alpha4beta2 nAChRs underlies nicotine dependence PubMed:21482353
a4b2-nAChRs have been implicated in nicotine self-administration, reward, and depen- dence, and in diseases such as Alzheimer’s and epilepsy [1–5,27–33]. PubMed:21787755
b4 subunit mRNA colocalizes with a4 subunit mRNA in many brain regions [37,38] that could be involved in complex behaviors including nicotine dependence. PubMed:21787755
This makes the hypothesis particularly intriguing that a6*-nAChRs play roles in nicotine dependence. PubMed:21787755
Human genetic studies have shown that the non- synonymous coding SNP D398N is associated with lung cancer and nicotine dependence PubMed:28901280
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