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Background: Both the high-risk human papillomavirus (HR-HPV) infection and tobacco exposure are significantly associated with cervical neoplasm risk. Immune cells play important roles in carcinogenesis. However, it is still unclear whether immune cells have a mediating effect on the HR-HPV infection and tobacco exposure with cervical neoplasm development. Aim: The aim of this study was to determine how the increased white blood cell (WBC) count affects the relationship between HR-HPV DNA load and tobacco exposure in the development of cervical neoplasia. Methods: A hospital-based case–control study design was conducted with a total of 108 cases of Taiwanese women with ≥ cervical intraepithelial neoplasia (CIN) I confirmed by biopsy, and 222 healthy Taiwanese female subjects with negative findings on a Pap smear were assigned to the control group. The study evaluated HR-HPV status and immune cell counts (WBCs, natural killer (NK) cells) and tobacco exposure by a self-construct questionnaire. Results: Both HR-HPV DNA load and tobacco exposure significantly independently increased cervical neoplasm risk (AORs: 1.28 and 1.42, respectively). Similar significant results were found for WBCs and NK cells, with respective AORs of 1.20 and 1.00. Moreover, increased WBCs (β = 0.04, 95% CI corrected: 0.01–0.07) and tobacco exposure (β = 0.02, 95% CI corrected: 0.01–0.04) mediated the relationship between the high-risk HPV DNA load and cervical neoplasm risk. Conclusions: Elevated WBC count acts as both predictor and mediator in cervical neoplasm development linked to HR-HPV DNA load. Monitoring and maintaining WBC levels within the normal range could be a preventive strategy for cervical neoplasm development. [ABSTRACT FROM AUTHOR]

This research analyzes immunological response patterns to SARS-CoV-2 infection in blood and urine in individuals with serum cotinine-confirmed exposure to nicotine. Samples of blood and urine were obtained from a total of 80 patients admitted to hospital within 24 h of admission (tadm), 48 h later (t48h), and 7 days later (t7d) if patients remained hospitalized or at discharge. Serum cotinine above 3.75 ng/mL was deemed as biologically significant exposure to nicotine. Viral load was measured with serum SARS-CoV-2 S-spike protein. Titer of IgG, IgA, and IgM against S- and N-protein assessed specific antiviral responses. Cellular destruction was measured by high mobility group box protein-1 (HMGB-1) serum levels and heat shock protein 60 (Hsp-60). Serum interleukin 6 (IL-6), and ferritin gauged non-specific inflammation. The immunological profile was assessed with O-link. Serum titers of IgA were lower at tadm in smokers vs. nonsmokers (p = 0.0397). IgM at t48h was lower in cotinine-positive individuals (p = 0.0188). IgG did not differ between cotinine-positive and negative individuals. HMGB-1 at admission was elevated in cotinine positive individuals. Patients with positive cotinine did not exhibit increased markers of non-specific inflammation and tissue destruction. The blood immunological profile had distinctive differences at admission (MIC A/B↓), 48 h (CCL19↓, MCP-3↓, CD28↑, CD8↓, IFNγ↓, IL-12↓, GZNB↓, MIC A/B↓) or 7 days (CD28↓) in the cotinine-positive group. The urine immunological profile showed a profile with minimal overlap with blood as the following markers being affected at tadm (CCL20↑, CXCL5↑, CD8↑, IL-12↑, MIC A/B↑, GZNH↑, TNFRS14↑), t48h (CCL20↓, TRAIL↓) and t7d (EGF↑, ADA↑) in patients with a cotinine-positive test. Here, we showed a distinctive immunological profile in hospitalized COVID-19 patients with confirmed exposure to nicotine. [ABSTRACT FROM AUTHOR]

BackgroundLung is the largest mucosal area of the human body and directly connected to the external environment, facing microbial exposure and environmental stimuli. Therefore, studying the internal microorganisms of the lung is crucial for a deeper understanding of the relationship between microorganisms and the occurrence and progression of lung cancer.MethodsTumor and adjacent nontumor tissues were collected from 38 lung adenocarcinoma patients and used nanopore sequencing technology to sequence the 16s full-length sequence of bacteria, and combining bioinformatics methods to identify and quantitatively analyze microorganisms in tissues, as well as to enrich the metabolic pathways of microorganisms.Resultsthe microbial composition in lung adenocarcinoma tissues is highly similar to that in adjacent tissues, but the alpha diversity is significantly lower than that in adjacent tissues. The difference analysis results show that the bacterial communities of Streptococcaceae, Lactobacillaceae, and Neisseriales were significantly enriched in cancer tissues. The results of metabolic pathway analysis indicate that pathways related to cellular communication, transcription, and protein synthesis were significantly enriched in cancer tissue. In addition, clinical staging analysis of nicotine exposure and lung cancer found that Haemophilus, paralinfluenzae, Streptococcus gordonii were significantly enriched in the nicotine exposure group, while the microbiota of Cardiobactereae and Cardiobacterales were significantly enriched in stage II tumors. The microbiota significantly enriched in IA-II stages were Neisseriaeae, Enterobacteriales, and Cardiobacterales, respectively.ConclusionNanopore sequencing technology was performed on the full length 16s sequence, which preliminarily depicted the microbial changes and enrichment of microbial metabolic pathways in tumor and adjacent nontumor tissues. The relationship between nicotine exposure, tumor progression, and microorganisms was explored, providing a theoretical basis for the treatment of lung cancer through microbial targets.

Cardiovascular health (CVH) is a critical issue for global health. However, no previous study has determined the prevalence of cardiovascular risk factors based on the American Heart Association's (AHA) Life's Essential 8 (LE8). Therefore, we aimed to estimate the global prevalence of the eight cardiovascular risk factors identified in the LE8. A systematic search of systematic reviews with meta-analysis on cardiovascular risk factors covering data reported between 2000 and 2019 was conducted on PubMed, Epistemonikos, and the Cochrane Library until 1 May 2023. After applying exclusion criteria, 79 studies remained in the final selection for the narrative synthesis in the systematic review, of which 33 of them were used in the meta-analysis which included 2 555 639 participants from 104 countries. The overall pooled prevalence of cardiovascular risk factors was as follows: insufficient physical activity, 26.3% (95% CI 2.3%–63.4%), no adherence to a healthy diet, 34.1% (95% CI 5.8%–71.2%), nicotine exposure, 15.4% (95% CI 10.4%–21.2%), insufficient sleep quality, 38.5% (95% CI 14.0%–66.7%), obesity, 17.3% (95% CI 6.1%–32.6%), dyslipidemia, 34.1% (95% CI 33.8%–34.4%), diabetes, 12.0% (95% CI 7.0%–18.2%), and hypertension, 29.4% (95% CI 23.3%–35.8%). These results warrant prevention strategies aimed at reducing insufficient sleep quality, and no adherence to a healthy diet as leading cardiovascular risk factors worldwide. The high prevalence of hypertension among children and adults is concerning and should also be adequately addressed through global policies. [ABSTRACT FROM AUTHOR]

Objective: To compare the effects of electroacupuncture (EA) and moxibustion at Zusanli (ST 36) on the lung phenotype of rat offspring exposed to nicotine during the perinatal period. Methods: Pregnant Sprague-Dawley rats were randomly divided into 4 groups: the control group (saline only), the model group (nicotine only), the EA group (nicotine + EA at ST 36 acupoints bilaterally), and the moxibustion group (nicotine + moxibustion at ST 36 acupoints bilaterally). n = 6 rats per group. On postnatal day 21, the body weight, lung weight, and pulmonary function were determined and lung morphometry was performed. Peroxisome proliferator-activated receptor gamma and β-catenin levels in the lung tissue of offspring were also determined. Results: Perinatal nicotine exposure (PNE) results in decreased body and lung weights of offspring rats, abnormal lung tissue morphology, and significantly altered pulmonary function, showing an increase in total airway resistance and a decrease in tidal volume, minute ventilation, total airway compliance, and peak expiratory flow. Bilateral EA at ST 36 acupoints could block all of these perinatal nicotine-induced effects. Although moxibustion also had protective effects in nicotine-induced offspring lungs, some of these effects did not reach statistical significance, e.g., protection against the upregulation of β-catenin, the downregulation of PPARγ signaling, and the increase in peak expiratory flow. Conclusion: Maternal EA at ST 36 blocked the PNE-induced changes in key developmental signaling pathways, prevented the PNE-induced changes in lung morphology, and protected pulmonary function. Moxibustion at ST 36 showed similar but weaker protective effects against the PNE-induced changes in the exposed offspring. It is important to note that the mechanism underlying the protective effects of moxibustion at ST 36 may be different from those of EA at ST 36, and further research is needed to understand these differences.

This research analyzes immunological response patterns to SARS-CoV-2 infection in blood and urine in individuals with serum cotinine-confirmed exposure to nicotine. Samples of blood and urine were obtained from a total of 80 patients admitted to hospital within 24 h of admission (tadm), 48 h later (t48h), and 7 days later (t7d) if patients remained hospitalized or at discharge. Serum cotinine above 3.75 ng/mL was deemed as biologically significant exposure to nicotine. Viral load was measured with serum SARS-CoV-2 S-spike protein. Titer of IgG, IgA, and IgM against S- and N-protein assessed specific antiviral responses. Cellular destruction was measured by high mobility group box protein-1 (HMGB-1) serum levels and heat shock protein 60 (Hsp-60). Serum interleukin 6 (IL-6), and ferritin gauged non-specific inflammation. The immunological profile was assessed with O-link. Serum titers of IgA were lower at tadm in smokers vs. nonsmokers (p = 0.0397). IgM at t48h was lower in cotinine-positive individuals (p = 0.0188). IgG did not differ between cotinine-positive and negative individuals. HMGB-1 at admission was elevated in cotinine positive individuals. Patients with positive cotinine did not exhibit increased markers of non-specific inflammation and tissue destruction. The blood immunological profile had distinctive differences at admission (MIC A/B↓), 48 h (CCL19↓, MCP-3↓, CD28↑, CD8↓, IFNγ↓, IL-12↓, GZNB↓, MIC A/B↓) or 7 days (CD28↓) in the cotinine-positive group. The urine immunological profile showed a profile with minimal overlap with blood as the following markers being affected at tadm (CCL20↑, CXCL5↑, CD8↑, IL-12↑, MIC A/B↑, GZNH↑, TNFRS14↑), t48h (CCL20↓, TRAIL↓) and t7d (EGF↑, ADA↑) in patients with a cotinine-positive test. Here, we showed a distinctive immunological profile in hospitalized COVID-19 patients with confirmed exposure to nicotine.

BACKGROUND: Hypoglycemia in neonates is common and contributes to 4.0–5.8% of neonatal intensive care unit (NICU) admissions. In utero nicotine exposure is underexplored as a potential contributor to neonatal hypoglycemia. Rat models have shown that in utero nicotine exposure can be associated with a reduction in pancreatic beta cell mass, leading to glucose dysregulation. The primary aim of this work is to study the risk of developing hypoglycemia after birth in a population of in utero nicotine-exposed neonates. METHODS: We conducted a retrospective matched cohort study that augmented an existing dataset of neonates admitted to a level IV NICU with household-based in utero nicotine exposure (N = 335). Neonates in the control group parents denied household smoking (N = 325), were born within a 6-month timeframe, and were within a birthweight of 50 grams of a nicotine-exposed neonate. Data reviewed included gestational age, growth parameters, maternal history of diabetes, and glucose levels within the first three hours of life per unit protocol. RESULTS: 660 neonates were included in the analysis. In utero nicotine exposure demonstrated a 94.3% posterior probability (PP) for greater hypoglycemia risk (RR = 1.185, 95% CrI = [0.953, 1.445]). A 94.6% PP was demonstrated when neonates who were small for gestational age, intrauterine growth-restricted, and born to diabetic mothers were excluded (n = 482; RR = 1.271, 95% CrI = [0.946, 1.669]). CONCLUSION: Nicotine exposure in utero was found to be a potential risk factor for developing hypoglycemia after birth. Mechanisms of action should be explored, and additional research on in utero nicotine exposure risks should follow. [ABSTRACT FROM AUTHOR]

Abstract:Aims: The consumption of alcohol and nicotine during pregnancy relate to a multitude of personal and socioeconomic factors. Since even the consumption in non-clinical populations pose a health risk to children, epidemiologic data related to factors potentially contributing to an increase in consumption during pregnancy were investigated. Methodology: Cross-sectional analyses were based on interview data from 260 pregnant women taking part in a longitudinal intervention project (Bremer Initiative to Foster Early Child Development). Women had a below-average family income, a migration background, or faced other social and cultural challenges. Descriptive statistics were calculated to determine consumption prevalence. Logistic regression models were conducted to estimate associations of alcohol or nicotine consumption with personal and socioeconomic factors. Results: Of the total sample (mean age: 31.1 years), 45 % consumed alcohol and/or nicotine during pregnancy. 92.3 % quit drinking and 62.8 % stopped smoking following confirmation of pregnancy. Better social support and higher age increased the likelihood of alcohol consumption, while this was decreased by an Islamic cultural background. Smoking was predicted by a lower level of education. Unplanned pregnancies predicted the consumption of both, alcohol and nicotine. Conclusions: A multitude of factors influence alcohol and nicotine consumption in non-clinical populations. Preventive strategies should include pre-pregnancy stages and health information needs to mirror factors contributing to consumption. [ABSTRACT FROM AUTHOR]

Early nicotine exposure compromises offspring's phenotype at long-term in both sexes. We hypothesize that offspring exposed to nicotine during breastfeeding show deregulated central and peripheral endocannabinoid system (ECS), compromising several aspects of their metabolism. Lactating rats received nicotine (NIC, 6 mg/Kg/day) or saline from postnatal day (PND) 2 to 16 through implanted osmotic minipumps. Offspring were analyzed at PND180. We evaluated protein expression of N-acylphosphatidylethanolamide-phospholipase D (NAPE-PLD), fatty acid amide hydrolase (FAAH), diacylglycerol lipase (DAGL), monoacylglycerol lipase (MAGL) and cannabinoid receptors (CB1 and/or CB2) in lateral hypothalamus, paraventricular nucleus of the hypothalamus, liver, visceral adipose tissue (VAT), adrenal and thyroid. NIC offspring from both sexes did not show differences in hypothalamic ECS markers. Peripheral ECS markers showed no alterations in NIC males. In contrast, NIC females had lower liver DAGL and CB1, higher VAT DAGL, higher adrenal NAPE-PLD and higher thyroid FAAH. Endocannabinoids biosynthesis was affected by nicotine exposure during breastfeeding only in females; alterations in peripheral tissues suggest lower action in liver and higher action in VAT, adrenal and thyroid. Effects of nicotine exposure during lactation on ECS markers are sex- and tissue-dependent. This characterization helps understanding the phenotype of the adult offspring in this model and may contribute to the development of new pharmacological targets for the treatment of several metabolic diseases that originate during development. [ABSTRACT FROM AUTHOR]

Amaç: Sigara, halk sağlığını tehdit eden ve tüm dünyada yaygın olarak kullanılan, en önemli önlenebilir ölüm nedenidir. Nikotin tütünde önemli bir toksik bileşen olup birçok kronik hastalığın patogenezine katkıda bulunur. Bu çalışmanın amacı, nikotin ile indüklenmiş nefrotoksisitede böbrek fonksiyonları, oksidatif DNA hasarı, apoptoz ve PARP yolağının olası rolünün araştırılmasıdır. Yöntem: Bu çalışmada, 24 adet C57BL6J soy erkek fare kontrol, salin ve nikotin olmak üzere üç gruba ayrılmıştır. Nikotin grubu farelere 14 gün boyunca günde 2 kere 3 mg/kg dozunda nikotin subkutan olarak enjekte edilmiştir. Salin grubuna aynı yöntemle serum fizyolojik sıvısı enjekte edilmiştir. Kontrol grubuna deneyin son gününe kadar hiçbir işlem uygulanmamıştır. Deneyin son günü farelerin kardiyak kan örnekleri alınmış ve bilateral böbrek dokuları izole edilmiştir. Kan örneklerinde ELISA yöntemiyle 8-OHdG ve kotinin düzeyleri ölçülmüştür. Sağ böbrek dokuları %10'luk formalin solüsyonunda fikse edilip parafin bloklara gömülmüştür. Kesitlere morfolojik değerlendirme için hematoksilen - eozin boyama yapılmıştır. Sol böbrek dokularında gerçek zamanlı kantitaif polimeraz zincir reaksiyonu yöntemiyle kaspaz-3 ve PARP-1 gen ekspresyon düzeyleri belirlenmiştir. Bulgular: Nikotin grubunda vücut ve böbrek ağırlığı anlamlı düzeyde azalmıştır (P<0.05). Serum 8-OHdG seviyesi nikotin grubunda kontrol ve salin gruplarına kıyasla anlamlı düzeyde artmıştır (P<0.05). Serum kotinin seviyesi nikotin grubunda 303.11±0.3 ng/ml olarak ölçülmüştür. Morfolojik değerlendirmede, nikotin grubunda glomerül çapında ve mezangial matrikste artış olduğu gözlenmiştir. Ayrıca, nikotin grubunda tübüler dilatasyon gözlenmiştir. Kaspaz-3 ve PARP-1 gen ekspresyon düzeyi nikotin grubunda kontrol ve salin gruplarına kıyasla anlamlı düzeyde artmıştır (P<0.05). Sonuç: Sonuç olarak, nikotin maruziyetinin böbrek dokusunda oksidatif DNA hasarını artırdığı ve hücre içi apoptoz ve PARP yolağını indüklediği saptanmıştır. Objective: Smoking is one of the most important preventable cause of death that threatens public health and is widely used all over the world. Nicotine is an important toxic component in tobacco and contributes to the pathogenesis of many chronic diseases. The aim of this study is to investigate the possible role of kidney functions, oxidative DNA damage, apoptosis and PARP pathway in nicotine-induced nephrotoxicity. Methods: 24 male C57BL6J mice were divided into control, saline and nicotine groups. Nicotine group mice were injected subcutaneously with nicotine at a dose of 3 mg/kg twice a day for 14 days. The saline group was injected with physiological saline. No procedure was performed to the control group. At the end of the experiment, cardiac blood samples and bilateral kidney tissues were isolated. The levels of 8-OHdG and cotinine were measured in serum by ELISA method. Hematoxylin - eosin staining was performed to right kidney tissues for morphological evaluation. Caspase-3 and PARP-1 gene expression levels were determined by real-time quantitative polymerase chain reaction method in left kidneys. Results: Body and kidney weights decreased significantly in nicotine group (P<0.05). Serum 8-OHdG level was significantly increased in nicotine group (P<0.05). Serum cotinine level was measured as 303.11±0.3 ng/ml in nicotine group. Glomerular diameter and mesangial matrix were increased in nicotine group. In addition, tubular dilatation was observed in nicotine group. Caspase-3 and PARP-1 gene expression levels were significantly increased in the nicotine group compared to the control and saline groups (P<0.05). Conclusion: In conclusion, it was determined that nicotine exposure increased oxidative DNA damage in kidney tissue and induced intracellular apoptosis and PARP pathway. [ABSTRACT FROM AUTHOR]

Tobacco-derived nicotine exposure is linked to depression. However, the associations of nicotine and its metabolites with symptoms of depression, particularly concerning gender differences, remain underexplored. The characteristics and total nicotine equivalents (TNE) of 1001 subjects were determined. The association between the TNE and symptoms of depression, accounting for gender differences, was investigated using generalized linear models and subgroup analyses. Men exhibited significantly greater levels of the nicotine exposure indicators TNE2, TNE3, TNE6, and TNE7 (P < 0.005). A significantly greater percentage of women (23.45 %) than men (9.81 %) exhibited symptoms of depression (P < 0.0001). In women, the relationship between the TNE and depression was reflected by a U-shaped curve with significant inflection points, particularly for TNE3, TNE6, and TNE7. Furthermore, in women, concentrations above 48.98 nmol/mL for TNE3, 53.70 nmol/mL for TNE6, and 57.54 nmol/mL for TNE7 were associated with 154 %, 145 %, and 138 % increases in the risk of depression, respectively. In contrast, these associations did not reach significance among men. The cross-sectional design limits the ability to infer causality between nicotine exposure and depressive symptoms. Larger-scale studies are needed to confirm these findings. Gender could be a significant factor influencing the relationship between nicotine exposure levels and symptoms of depression. The impact of nicotine exposure on symptoms of depression should be particularly considered among women. This study revealed the complex relationship between tobacco-related nicotine exposure and depressive symptoms, with a particular focus on gender differences. Our results revealed a distinct U-shaped correlation between total nicotine equivalents and depression in women, which differed from that in men. These findings emphasize the importance of tailoring clinical approaches to address nicotine exposure and manage depressive symptoms based on gender. [Display omitted] • Identified U-shaped correlation in women • No discernible pattern detected in men • Women may be more sensitive to nicotine • TNE risk thresholds for women [ABSTRACT FROM AUTHOR]

In the United States, the Food and Drug Administration (FDA) has initiated a public dialogue about reducing the nicotine content of cigarettes. A reduced-nicotine standard could increase withdrawal symptoms among current smokers. We examined the impact of switching smokers to cigarettes that varied in nicotine content on withdrawal symptoms over 6 weeks. A secondary analysis (N = 839) of a 10-site, double-blind clinical trial of nontreatment-seeking smokers was completed. Participants were instructed to smoke study cigarettes, containing 0.4 to 15.8 mg of nicotine/g of tobacco, for 6 weeks and were then abstinent overnight. Using latent growth curves, trajectories of individual withdrawal symptoms were compared between the reduced nicotine content (RNC) conditions and a normal nicotine content (NNC) condition. Path analyses compared symptoms after overnight abstinence. Relative to NNC cigarettes, participants smoking RNC cigarettes had increased anger/irritability/frustration and increased appetite/weight gain during the initial weeks, but the symptoms resolved by Week 6. Individuals who were biochemically verified as adherent with using only the 0.4 mg/g cigarettes had higher sadness levels (Cohen's d = .40) at Week 6 compared with the NNC condition, although symptoms were mild. After a post-Week 6 overnight abstinence challenge, some RNC conditions relative to NNC condition exhibited reduced withdrawal. Individuals who were biochemically confirmed as adherent to the lowest nicotine condition experienced only mild and transient symptom elevations. Thus, a reduced-nicotine standard for cigarettes produced a relatively mild and temporary increase in withdrawal among nontreatment-seeking smokers (ClinicalTrials.gov No. NCT01681875). (PsycINFO Database Record

Children of mothers who smoked during pregnancy are at significantly greater risk for cognitive impairments including memory deficits, but the mechanisms underlying this effect remain to be understood. In rodent models of smoking during pregnancy, early postnatal nicotine exposure results in impaired long-term hippocampus-dependent memory, functional loss of α2-containing nicotinic acetylcholine receptors (α2∗ nAChRs) in oriens-lacunosum moleculare (OLM) cells, increased CA1 network excitation, and unexpected facilitation of long-term potentiation (LTP) at Schaffer collateral-CA1 synapses. Here we demonstrate that α2 knockout mice show the same pattern of memory impairment as previously observed in wild-type mice exposed to early postnatal nicotine. However, α2 knockout mice and α2 knockout mice exposed to early postnatal nicotine did not share all of the anomalies in hippocampal function observed in wild-type mice treated with nicotine during development. Unlike nicotine-treated wild-type mice, α2 knockout mice and nicotine-exposed α2 knockout mice did not demonstrate increased CA1 network excitation following Schaffer collateral stimulation and facilitated LTP, indicating that the effects are likely adaptive changes caused by activation of α2∗ nAChRs during nicotine exposure and are unlikely related to the associated memory impairment. Thus, the functional loss of α2∗ nAChRs in OLM cells likely plays a critical role in mediating this developmental-nicotine-induced hippocampal memory deficit.

Abstract Background Over one-quarter of all smokers in the United States identify as non-daily smokers and this number is projected to rise. Unlike daily smokers who typically maintain consistent levels of nicotine exposure with regular smoking, non-daily smokers have variable patterns of smoking that likely result in high intraindividual variability in nicotine intake. The current study aimed to characterize the weekly intraindividual variability in cotinine and identify smoking-related predictors in nondaily smokers. Methods An ecological momentary assessment of 60 non-daily smokers ages 24–57 years was conducted over a consecutive 7-day at-home protocol to log each smoking session, assessments of mood and social activity during smoking, and collection of daily saliva samples in a convenience sample from Pennsylvania, USA. Hierarchical linear regression analyses were conducted to determine the effects of smoking characteristics on total cotinine exposure measured by pharmacokinetic area under the curve and the range, maximum, and minimum cotinine values during the week controlling for demographic variables. Results The mean daily cotinine level was 119.2 ng/ml (SD = 168.9) with individual values that ranged from nondetectable to 949.6 ng/ml. Menthol predicted increased total cotinine levels (P

Background: Lung is the largest mucosal area of the human body and directly connected to the external environment, facing microbial exposure and environmental stimuli. Therefore, studying the internal microorganisms of the lung is crucial for a deeper understanding of the relationship between microorganisms and the occurrence and progression of lung cancer., Methods: Tumor and adjacent nontumor tissues were collected from 38 lung adenocarcinoma patients and used nanopore sequencing technology to sequence the 16s full-length sequence of bacteria, and combining bioinformatics methods to identify and quantitatively analyze microorganisms in tissues, as well as to enrich the metabolic pathways of microorganisms., Results: the microbial composition in lung adenocarcinoma tissues is highly similar to that in adjacent tissues, but the alpha diversity is significantly lower than that in adjacent tissues. The difference analysis results show that the bacterial communities of Streptococcaceae , Lactobacillaceae , and Neisseriales were significantly enriched in cancer tissues. The results of metabolic pathway analysis indicate that pathways related to cellular communication, transcription, and protein synthesis were significantly enriched in cancer tissue. In addition, clinical staging analysis of nicotine exposure and lung cancer found that Haemophilus , paralinfluenzae , Streptococcus gordonii were significantly enriched in the nicotine exposure group, while the microbiota of Cardiobactereae and Cardiobacterales were significantly enriched in stage II tumors. The microbiota significantly enriched in IA-II stages were Neisseriaeae , Enterobacteriales , and Cardiobacterales , respectively., Conclusion: Nanopore sequencing technology was performed on the full length 16s sequence, which preliminarily depicted the microbial changes and enrichment of microbial metabolic pathways in tumor and adjacent nontumor tissues. The relationship between nicotine exposure, tumor progression, and microorganisms was explored, providing a theoretical basis for the treatment of lung cancer through microbial targets., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Yang, Wang, Ding, Zhang, Zhu, Wang, Pan, Li, Wang and Yu.)

Introduction: COVID-19 (or COVID) is a highly virulent viral disease which more frequently presents severe infection in specific populations, such as the elderly, patients with hypertension, patients with respiratory disease, and patients who smoke. The effects vaping (i.e., an electronic cigarette or JUUL device) has on COVID progression remains unclear, because there is an information paucity correlating e-cigarette use and COVID. This review sought to identify links between vape use and COVID severity via literature review. Additionally, because there is more widespread information about cigarette smoking than about vaping, this review sought to illustrate commonalities between smoking and vaping. If smoking and vaping are deemed near-identical practices, then it is possible the effects of smoking on human health and on COVID disease could be comparable in vaping. Methods: Several searches were performed on PubMed with MeSH headings and JSTOR between 17 December 2020 and 22 December 2020. Search results were excluded if they were not trials or controlled clinical trials, if the articles were not about COVID, if the articles were about smoking behaviors or habits, or if the articles were not related to vaping or smoking. Key findings were summarized and tabled based on relevance, substantiability, and applicability to COVID. Results: Multiple sources viewed smoking and vaping as equal risk factors for COVID disease, whereas other sources viewed the two as unique risk factors. Because of this controversy, it is challenging to view the two practices as similar enough to pose equivalent risks for COVID. Both practices pose significant health risks to its users, but these health risks are unique to each practice. Discussion: There are several limitations which exacerbate ambiguity--(1) it is unclear how harmful smoking is for COVID patients, because several publications found smoking may have protective effects; (2) few older patients vape, but yet most severe COVID cases occur in older populations; (3) older patients and impoverished patients show a statistically significant risk for severe COVID disease independent of other factors; (4) vaping is a relatively new practice, and there are few patients who self-report long-term e-cigarette use or long-term adverse effects as a result thereof. Conclusion: Although vaping may present serious health risks, clinically, it is uncertain how significantly vaping affects COVID disease, especially when compared against cigarette smoking. More research is needed on both the effects of vaping on COVID and the likeness of vaping versus smoking. [ABSTRACT FROM AUTHOR]

Background: Active smoking and exposure to environmental tobacco smoke may be related to cognitive function decline. We assessed the associations of urinary levels of nicotine and its metabolites with cognitive function. Methods: A total of 553 elder adults at high risk of cognitive impairment and 2212 gender- and age-matched individuals at low risk of cognitive impairment were selected at a ratio of 1: 4 from the remained individuals (n = 6771) who completed the baseline survey of the Shenzhen Ageing-Related Disorder Cohort, after excluding those with either Alzheimer’s disease, Parkinson’s syndrome or stroke as well as those with missing data on variables (including active and passive smoking status, Mini-Cog score). Urinary levels of nicotine and its metabolites and cognitive function for all individuals were measured by high-performance liquid chromatography-tandem mass spectrometry (LC-MS/MS) and assessed using the Mini-Cog test, respectively. Associations of urinary levels of nicotine and its metabolites with cognitive function were analyzed by conditional logistic regression models. Results: Individuals in the highest tertile of urinary OHCotGluc (OR: 1.52, 95%CI: 1.19–1.93) or NNO (OR: 1.50, 95%CI: 1.16–1.93) levels as well as in the second tertile of urinary ∑Nic level (OR: 1.43, 95%CI: 1.13–1.82) were at higher risk of cognitive impairment compared with those in the corresponding lowest tertile. Restricted cubic spline models revealed the non-linear dose-response relationships between urinary levels of OHCotGluc, NNO or ∑Nic and the risk of cognitive impairment. Conclusions: Urinary levels of OHCotGluc, NNO or ∑Nic exhibited a non-linear dose-response relationship with cognitive function in the urban elderly.

Background: Over one-quarter of all smokers in the United States identify as non-daily smokers and this number is projected to rise. Unlike daily smokers who typically maintain consistent levels of nicotine exposure with regular smoking, non-daily smokers have variable patterns of smoking that likely result in high intraindividual variability in nicotine intake. The current study aimed to characterize the weekly intraindividual variability in cotinine and identify smoking-related predictors in nondaily smokers.Methods: An ecological momentary assessment of 60 non-daily smokers ages 24-57 years was conducted over a consecutive 7-day at-home protocol to log each smoking session, assessments of mood and social activity during smoking, and collection of daily saliva samples in a convenience sample from Pennsylvania, USA. Hierarchical linear regression analyses were conducted to determine the effects of smoking characteristics on total cotinine exposure measured by pharmacokinetic area under the curve and the range, maximum, and minimum cotinine values during the week controlling for demographic variables.Results: The mean daily cotinine level was 119.2 ng/ml (SD = 168.9) with individual values that ranged from nondetectable to 949.6 ng/ml. Menthol predicted increased total cotinine levels (P < 0.05). Shorter time to the first cigarette of the day predicted significantly higher minimum (P < 0.05), maximum (P < 0.05), and total cotinine values (P < 0.05) after controlling for covariates. Negative emotions and social interactions with others were also significantly associated with higher cotinine metrics. There was no significant effect of the nicotine metabolite ratio.Conclusions: Our findings highlight the variability in nicotine exposure across days among non-daily smokers and point to the role of smoking context in nicotine exposure. The findings suggest the need to develop better assessment methods to determine health and dependence risk and personalized cessation interventions for this heterogeneous and growing group of smokers. [ABSTRACT FROM AUTHOR]

Aim: We systematically reviewed the literature on the influence of low and moderate amounts of prenatal alcohol and nicotine exposure on early child development. This paper also suggests possible directions for future research in order to tackle the controversial findings identified. Methods: The PubMed and Web of Science electronic databases were searched together with the reference lists of the selected papers. Empirical studies were included if they focused on the effects of low or moderate exposure, reported outcomes on child development within the first 2 years of life and were published in English between January 2009 and December 2019. The eligibility of the included studies was based on three authors reading the full text. Results: The final sample comprised 17 papers. Of these, 13 focused on the effects of prenatal alcohol exposure and they reported decreased sensory sensibility, smaller body sizes and increased cognitive capacities. The other four looked at prenatal nicotine exposure, and they primarily found impairments in children's orienting, communication and motor skills. Conclusion: Any amount of prenatal alcohol and nicotine exposure appeared to risk healthy child development. There were many reasons for consumption and numerous effects on the child, but representative data from interdisciplinary research were missing. [ABSTRACT FROM AUTHOR]

Objectives: To observe the effects of electroacupuncture(EA) on memory, cognitive impairment, and the brain-derived neurotrophic factor(BDNF)/N-methyl-D-aspartate receptor subtype 1(NMDAR1) pathway in the brains of offspring rat with intrauterine growth restriction(IUGR) induced by perinatal nicotine exposure(PNE), so as to explore the underlying mechanism., Methods: SD rats were randomly divided into normal, model, and EA groups, with 4 mothers and 10 offspring rats of each mother in each group. The IUGR model was established by subcutaneous injection of nicotine during pregnancy and lactation. From the 6 th day of pregnancy in the mothers until the 21 st day after birth of the offspring rats, EA (2 Hz/15 Hz, 1 mA) was administered bilaterally at the "Zusanli"(ST36) of mothers, once daily for 20 min. The brain organ coefficient was used to evaluate the brain development of the offspring rats. The Y-maze test and novel object recognition experiments were performed to assess memory and cognitive function. HE staining was used to observe the development and cellular morphology of the hippocampus and prefrontal cortex in the offspring rats. UV spectrophotometry was used to measure the glutamate(Glu) content in the hippocampus. ELISA was used to detect the BDNF content in the hippocampus. Western blot was performed to measure the protein expression of NMDAR1 in the hippocampus. Immunohistochemistry was used to count the number of BDNF-positive cells in the hippocampus and prefrontal cortex., Results: Compared with the normal group, the brain organ coefficient, exploration time of the novel arm, spontaneous alternation rate, and novel object recognition index, contents of BDNF and expression of NMDAR1 proteins in the hippocampus, the number of BDNF-positive cells in the CA1 and CA3 regions of the hippocampus and prefrontal cortex were significantly reduced( P <0.01), while the Glu content in the hippocampus was significantly increased( P <0.01) in the model group of offspring rats；decreased cell number, scattered arrangement, and disrupted cellular structure were observed in the hippocampus and prefrontal cortex of offspring rats in the model group. Compared with the model group, the brain organ coefficient, exploration time of the novel arm, spontaneous alternation rate, and novel object recognition index, the BDNF contents and NMDAR1 protein expression in the hippocampus, the number of BDNF-positive cells in the hippocampal CA1 and CA3 regions and prefrontal cortex significantly increased( P <0.01, P <0.05), while the Glu content in the hippocampus was significantly decreased ( P <0.01) in offspring rats of the EA group；increased cell number, neat arrangement, and reduced cellular damage were observed in the hippocampus and prefrontal cortex in the EA group., Conclusions: EA has an improving effect on memory and cognitive function impairment in offspring rats with IUGR induced by PNE, and this mechanism may be associated with the regulation of BDNF/NMDAR1 pathway, thereby improving the neuronal quantity and structure of the hippocampus and prefrontal cortex in offspring rats.

Nicotine decreases food intake, and smokers often report that they smoke to control their weight. To see whether similar phenomena could be observed in the model organism Caenorhabditis elegans, we challenged drug-naïve nematodes with a chronic low (0.01 mM) and high (1 mM) nicotine concentration for 55 h (from hatching to adulthood). After that, we recorded changes in their behavior in a nicotine gradient, where they could choose a desired nicotine concentration. By using a combination of behavioral and morphometric methods, we found that both nicotine and food modulate worm behavior. In the presence of food (E. coli OP50) the nematodes adapted to the low nicotine concentration, when placed in the gradient, chose a similar nicotine concentration like C. elegans adapted to the high nicotine concentration. However, in the absence of food, the nematodes adapted to the low nicotine concentration, when placed in the gradient of this alkaloid, chose a similar nicotine concentration like naïve worms. The nematodes growing up in the presence of high concentrations of nicotine had a statistically smaller body size, compared to the control condition, and the presence of food did not cause any enhanced slowing movement. These results provide a platform for more detailed molecular and cellular studies of nicotine addiction and food intake in this model organism. [ABSTRACT FROM AUTHOR]

Aim: In parallel with falling smoking rates, use of the oral moist tobacco product snus increases among women in reproductive age. We report an update on prevalence and effects of maternal use of snus and nicotine replacement therapy (NRT) during pregnancy and breastfeeding.Methods: A literature search of human studies in Medline, PubMed and EMBASE was conducted from September 2016 to May 2018, with stepwise screening of abstracts and subsequent relevant full-text papers for inclusion in Scandinavian and English languages.Results: Based on three studies, the prevalence of snus use in pregnancy was up to 3.4% in the first trimester and 2.1% in the third trimester. In 12 studies, we found increased risk of several adverse effects, especially preterm delivery, stillbirth and small for gestational age associated with maternal snus use during pregnancy. Knowledge on effects of NRT during pregnancy was conflicting and inconclusive in 10 studies. We did not identify any studies on prevalence or potential health effects of snus or NRT during breastfeeding.Conclusion: Few studies with updated data on the prevalence and adverse health effects of maternal use of snus and NRT during pregnancy were found. No studies during breastfeeding were identified. [ABSTRACT FROM AUTHOR]

The adolescent brain is vulnerable to long‐lasting cognitive disturbances resulting from nicotine exposure. Although exercise has been used as an intervention for ameliorating cognitive deficits in various disorders, the effect on cognitive changes induced by nicotine exposure and its underlying mechanisms remain unclear. The purpose of this study was to investigate the effects of exercise on nicotine reward‐associated cognitive behaviors in adolescent rats subjected to nicotine conditioned place preference paradigm (CPP). Male adolescent rats were trained on the Go/NoGo task, then subjected to nicotine CPP, and then randomly separated into four groups: sedentary (SED), high‐ (HE), moderate‐ (ME), and low‐intensity (LE) exercise. Rats in exercise groups performed treadmill running 30 min daily for 10 days. Results showed that MEs had shorter escape latencies in the Morris water maze (MWM) test compared to SEDs. Although time spent and distance swam in the target quadrant significantly increased in both the MEs and HEs, the number of target quadrant crosses increased significantly only in MEs. MEs and HEs showed higher performance accuracy on NoGo and lower scores on CPP tasks. Expression of α7 nicotinic acetylcholine receptors (nAChRs) and downstream signaling molecules increased in MEs in prefrontal cortex but not hippocampus, with α7 nAChRs expression positively associated with NoGo accuracy and MWM probe test performance, but negatively correlated with CPP scores. The findings of this study suggest that moderate‐intensity exercise can improve nicotine induced cognitive behaviors, and implicates prefrontal cortical α7 nAChR‐mediated signal transduction as a possible mechanism. [ABSTRACT FROM AUTHOR]

Nicotine is an addictive drug whose popularity has recently increased, particularly among adolescents, because of the availability of electronic nicotine devices (i.e., "vaping") and nicotine e-liquids containing additives with rich chemosensory properties. Some efforts to understand the role of these additives in nicotine reward suggest that they increase nicotine reward and reinforcement, but the sensory contributions of additives, especially in their vapor forms, are largely untested. Here, to better understand how a fruit-flavored (i.e., strawberry) additive influences nicotine reward and aversion, we used a conditioned place preference (CPP) procedure in which nicotine and a strawberry additive were delivered as a vapor to male and female adolescent mice. We found that nicotine vapor alone can lead to a dose-dependent CPP when using a biased design. The strawberry additive did not produce CPP on its own, and we did not observe an effect of the strawberry additive on nicotine vapor-induced reward. Nevertheless, mice exposed to nicotine plus strawberry additive vapor had higher plasma cotinine concentrations, which did not appear to reflect altered nicotine metabolism. Instead, by directly measuring vapor sampling through respiration monitoring, we uncovered an increase in the amount of sniffing toward strawberry-containing nicotine vapor compared with nicotine vapor alone. Together these data indicate that chemosensory-rich e-liquid additives may enhance the perceived sensory profile of nicotine vapors rather than the reward value per se, which leads to overall increased nicotine exposure., Competing Interests: The authors declare no competing financial interests., (Copyright © 2023 Patten et al.)