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Aldo Lorenzetti M.D, Internal Medicine & Hepatology, Milano - SIMEDET Delegate
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Increased Cardiac Sympathetic Activity and Oxidative Stress in Habitual Electronic #Cigarette Users
Implications for #Cardiovascular Risk

http://jamanetwork.com/journals/jamacardiology/article-abstract/2600166

Habitual electronic cigarette use is associated with physiologic effects. Further research into potential adverse health effects of electronic cigarettes is warranted
Increased Cardiac #Sympathetic Activity and Oxidative Stress in Habitual Electronic #Cigarette Users
Implications for Cardiovascular Risk

http://jamanetwork.com/journals/jamacardiology/article-abstract/2600166

In this study, habitual e-cigarette use was associated with a shift in cardiac autonomic balance toward sympathetic predominance and increased oxidative stress, both associated with increased cardiovascular risk.
Chronic #Cigarette Smoke-Induced #Epigenomic Changes Precede Sensitization of Bronchial Epithelial Cells to Single-Step Transformation by KRAS Mutations
http://www.cell.com/cancer-cell/fulltext/S1535-6108(17)30349-5

Highlights
•Chronic smoke exposure causes sequential chromatin changes leading to gene silencing
•Silenced genes are normally polycomb controlled but adopt abnormal DNA methylation
•Gene methylation causes sequential upregulation of key signal transduction pathways
•Epigenetic alterations sensitize cells to transformation by a single oncogenic event

We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells for transformation by a single oncogene. The smoke-induced chromatin changes include initial repressive polycomb marking of genes, later manifesting abnormal DNA methylation by 10 months. At this time, cells exhibit epithelial-to-mesenchymal changes, anchorage-independent growth, and upregulated RAS/MAPK signaling with silencing of hypermethylated genes, which normally inhibit these pathways and are associated with smoking-related non-small cell lung cancer. These cells, in the absence of any driver gene mutations, now transform by introducing a single KRAS mutation and form adenosquamous lung carcinomas in mice. Thus, epigenetic abnormalities may prime for changing oncogene senescence to addiction for a single key oncogene involved in lung cancer initiation
Low #cigarette consumption and risk of #coronary heart disease and #stroke: meta-analysis of 141 cohort studies in 55 study reports
http://www.bmj.com/content/360/bmj.j5855


The meta-analysis included 55 publications containing 141 cohort studies. Among men, the pooled relative risk for coronary heart disease was 1.48 for smoking one cigarette per day and 2.04 for 20 cigarettes per day, using all studies, but 1.74 and 2.27 among studies in which the relative risk had been adjusted for multiple confounders. Among women, the pooled relative risks were 1.57 and 2.84 for one and 20 cigarettes per day (or 2.19 and 3.95 using relative risks adjusted for multiple factors).

Men who smoked one cigarette per day had 46% of the excess relative risk for smoking 20 cigarettes per day (53% using relative risks adjusted for multiple factors), and women had 31% of the excess risk (38% using relative risks adjusted for multiple factors). For stroke, the pooled relative risks for men were 1.25 and 1.64 for smoking one or 20 cigarettes per day (1.30 and 1.56 using relative risks adjusted for multiple factors). In women, the pooled relative risks were 1.31 and 2.16 for smoking one or 20 cigarettes per day (1.46 and 2.42 using relative risks adjusted for multiple factors). The excess risk for stroke associated with one cigarette per day (in relation to 20 cigarettes per day) was 41% for men and 34% for women (or 64% and 36% using relative risks adjusted for multiple factors). Relative risks were generally higher among women than men.

Conclusions Smoking only about one cigarette per day carries a risk of developing coronary heart disease and stroke much greater than expected: around half that for people who smoke 20 per day. No safe level of smoking exists for cardiovascular disease. Smokers should aim to quit instead of cutting down to significantly reduce their risk of these two common major disorders
Association of E-#Cigarette Use With Smoking #Cessation Among Smokers Who Plan to Quit After a Hospitalization: A Prospective Study

http://annals.org/aim/article-abstract/2676738/association-e-cigarette-use-smoking-cessation-among-smokers-who-plan

Twenty-eight percent of participants used an e-cigarette within 3 months after discharge. In an analysis of 237 propensity score–matched pairs, e-cigarette users were less likely than nonusers to abstain from tobacco use at 6 months (10.1% vs. 26.6%; risk difference, −16.5% 95% CI, −23.3% to −9.6%). The association between e-cigarette use and quitting varied between intervention patients, who were given easy access to conventional treatment (7.7% vs. 29.8%; risk difference, −22.1% CI, −32.3% to −11.9%), and control patients, who received only treatment recommendations (12.0% vs. 24.1%; risk difference, −12.0% CI, −21.2% to 2.9%) (P for interaction = 0.143).

Conclusion:
During 3 months after hospital discharge, more than a quarter of smokers attempting to quit used e-cigarettes, mostly to aid cessation, but few used them regularly. This pattern of use was associated with less tobacco abstinence at 6 months than among smokers who did not use e-cigarettes. Additional study is needed to determine whether regular use of e-cigarettes aids or hinders smoking cessation.
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Acute Effects of Electronic #Cigarette Aerosol Inhalation on #Vascular Function Detected at Quantitative MRI

https://pubs.rsna.org/doi/10.1148/radiol.2019190562

Previous studies showed that nicotinized electronic cigarettes (hereafter, e-cigarettes) elicit systemic oxidative stress and inflammation. However, the effect of the aerosol alone on endothelial function is not fully understood.

Thirty-one healthy never-smokers (mean age, 24.3 years ± 4.3; 14 women) were evaluated. After e-cigarette vaping, resistivity index was higher (0.03 of 1.30 [2.3%]; P < .05), luminal flow-mediated dilation severely blunted (−3.2% of 9.4% [−34%]; P < .001), along with reduced peak velocity (−9.9 of 56.6 cm/sec [−17.5%]; P < .001), hyperemic index (−3.9 of 15.1 cm/sec2 [−25.8%]; P < .001), and delayed time to peak (2.1 of 7.1 sec [29.6%]; P = .005); baseline SvO2 was lower (−13 of 65 %HbO2 [−20%]; P < .001) and overshoot higher (10 of 19 %HbO2 [52.6%]; P < .001); and aortic pulse wave velocity marginally increased (0.19 of 6.05 m/sec [3%]; P = .05). Remaining parameters did not change after aerosol inhalation.

Conclusion
Inhaling nicotine-free electronic cigarette aerosol transiently impacted endothelial function in healthy nonsmokers. Further studies are needed to address the potentially adverse long-term effects on vascular health.
Electronic-#cigarette smoke induces #lung adenocarcinoma and #bladder urothelial hyperplasia in mice

Electronic-cigarettes (E-cigs) are marketed as a safe alternative to tobacco to deliver the stimulant nicotine, and their use is gaining in popularity, particularly among the younger population. We recently showed that mice exposed to short-term (12 wk) E-cig smoke (ECS) sustained extensive DNA damage in lungs, heart, and bladder mucosa and diminished DNA repair in lungs..

..We found that mice exposed to ECS for 54 wk developed lung adenocarcinomas (9 of 40 mice, 22.5%) and bladder urothelial hyperplasia (23 of 40 mice, 57.5%). These lesions were extremely rare in mice exposed to vehicle control or filtered air. Current observations that ECS induces lung adenocarcinomas and bladder urothelial hyperplasia, combined with our previous findings that ECS induces DNA damage in the lungs and bladder and inhibits DNA repair in lung tissues, implicate ECS as a lung and potential bladder carcinogen in mice. While it is well established that tobacco smoke poses a huge threat to human health, whether ECS poses any threat to humans is not yet known and warrants careful investigation.

https://bit.ly/35TzTAE
Association of #Cigarette Smoking With Antineutrophil Cytoplasmic Antibody–Associated #Vasculitis
https://2medical.news/2020/04/23/association-of-cigarette-smoking-with-antineutrophil-cytoplasmic-antibody-associated-vasculitis/

Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a systemic small vessel vasculitis characterized by circulating ANCAs targeting proteinase 3 (PR3) or myeloperoxidase (MPO) and associated with excess morbidity and mortality. Myeloperoxidase-ANCA–positive AAV and PR3-ANCA–positive AAV are increasingly recognized to have differences in genetic risk, pathogenesis, and response to treatment. Risk factors for AAV, including cigarette smoking, are poorly understood.. ..Overall, 473 cases were matched with …