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INTRODUCTION: The global tobacco epidemic poses a notable challenge to global health due to its association with various tobacco-related diseases. Although tobacco smoking is associated with depression, the exact mechanism by which tobacco smoking increases the risk of depression is unclear. This study explored the potential effects of tobacco smoking on depression. METHODS: We used data in the analysis from the Taiwan Biobank of 27916 individuals recruited from 2015 to 2020. To investigate the associations between tobacco use and depression, the results of the depression-measuring subscale of the Patient Health Questionnaire-4 as well as data on participants' tobacco consumption and other relevant covariates, were analyzed. RESULTS: Participants who smoked were more likely to report depression than those who did not smoke (AOR=1.50; 95% CI: 1.21-1.86). Furthermore, depression was significantly higher in women who smoked than in their male counterparts (females: AOR=1.68; 95% CI: 1.27-2.23, and males: AOR=1.32; 95% CI: 0.96-1.80). Women aged <55 years and who smoked were more likely to report depression, whereas this trend was not observed in those aged ≥55 years (<55 years: AOR=1.75; 95% CI: 1.23-2.48), and ≥55 years: AOR=1.58; 95% CI: 0.97-2.56). CONCLUSIONS: Tobacco smoking is a significant factor associated with depression, particularly in younger women. The increasing prevalence of tobacco use for years among younger women in Taiwan might contribute to shifts in the associations between depression and tobacco use in women.
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Heart failure (HF) and cancer have similar risk factors. HMG-CoA reductase inhibitors, also known as statins, are chemoprotective agents against carcinogenesis. We aimed to evaluate the chemoprotective effects of statins against liver cancer in patients with HF. This cohort study enrolled patients with HF aged ≥20 years between 1 January 2001 and 31 December 2012 from the National Health Insurance Research Database in Taiwan. Each patient was followed to assess liver cancer risk. A total of 25,853 patients with HF were followed for a 12-year period; 7364 patients used statins and 18,489 did not. The liver cancer risk decreased in statin users versus non-users (adjusted hazard ratio (aHR) = 0.26, 95% confidence interval (CI): 0.20-0.33) in the entire cohort in the multivariate regression analysis. In addition, both lipophilic and hydrophilic statins reduced the liver cancer risk in patients with HF (aHR 0.34, 95% CI: 0.26-0.44 and aHR 0.42, 95% CI: 0.28-0.54, respectively). In the sensitivity analysis, statin users in all dose-stratified subgroups had a reduced liver cancer risk regardless of age, sex, comorbidity, or other concomitant drug use. In conclusion, statins may decrease liver cancer risk in patients with HF.
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The gradual accumulation of mitochondrial DNA (mtDNA) mutations is implicated in aging and may contribute to the accelerated aging phenotype seen with tobacco smoking and HIV infection. mtDNA mutations are thought to arise from oxidative damage; however, recent reports implicate polymerase γ errors during mtDNA replication. Investigations of somatic mtDNA mutations have been hampered by technical challenges in measuring low-frequency mutations. We use primer ID-based next-generation sequencing to quantify both somatic and heteroplasmic blood mtDNA point mutations within the D-loop, in 164 women and girls aged 2-72 years, of whom 35% were smokers and 56% were HIV-positive. Somatic mutations and the occurrence of heteroplasmic mutations increased with age. While transitions are theorized to result from polymerase γ errors, transversions are believed to arise from DNA oxidative damage. In our study, both transition and transversion mutations were associated with age. However, transition somatic mutations were more prevalent than transversions, and no heteroplasmic transversions were observed. We also measured elevated somatic mutations, but not heteroplasmy, in association with high peak HIV viremia. Conversely, heteroplasmy was higher among smokers, but somatic mutations were not, suggesting that smoking promotes the expansion of preexisting mutations rather than de novo mutations. Taken together, our results are consistent with blood mtDNA mutations increasing with age, inferring a greater contribution of polymerase γ errors in mtDNA mutagenesis. We further suggest that smoking and HIV infection both contribute to the accumulation of mtDNA mutations, though in different ways.
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Envelhecimento/genética , DNA Mitocondrial/genética , Infecções por HIV/genética , Mutação , Fumar/genética , Adolescente , Adulto , Criança , Pré-Escolar , Feminino , Sequenciamento de Nucleotídeos em Larga Escala , Humanos , Lactente , Masculino , Pessoa de Meia-Idade , Adulto JovemRESUMO
Two new seco-sativene sesquiterpenoids, bipolenins D (1) and E (2), a new seco-longifolene sesquiterpenoid, bipolenin F (3), together with three known analogues (4-6), were obtained from cultures of endophytic fungus Bipolaris eleusines. Their structures were established by MS and NMR data. Compounds 1-6 showed no activity to five human cancer cell lines.
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Natural products play an important role in promoting health with relation to the prevention of chronic inflammation. N(6)-(2-Hydroxyethyl)adenosine (HEA), a physiologically active compound in the medicinal mushroom Cordyceps cicadae, has been identified as a Ca(2+) antagonist and shown to control circulation and possess sedative activity in pharmacological tests. The fruiting body of C. cicadae has been widely applied in Chinese medicine. However, neither the anti-inflammatory activities of HEA nor the fruiting bodies of C. cicadae have been carefully examined. In this study, we first cultured the fruiting bodies of C. cicadae and then investigated the anti-inflammatory activities of water and methanol extracts of wild and artificially cultured C. cicadae fruiting bodies. Next, we determined the amount of three bioactive compounds, adenosine, cordycepin, and HEA, in the extracts and evaluated their synergistic anti-inflammatory effects. Moreover, the possible mechanism involved in anti-inflammatory action of HEA isolated from C. cicadae was investigated. The results indicate that cordycepin is more potent than adenosine and HEA in suppressing the lipopolysaccharide (LPS)-stimulated release of pro-inflammatory cytokines by RAW 264.7 macrophages; however, no synergistic effect was observed with these three compounds. HEA attenuated the LPS-induced pro-inflammatory responses by suppressing the toll-like receptor (TLR)4-mediated nuclear factor-κB (NF-κB) signaling pathway. This result will support the use of HEA as an anti-inflammatory agent and C. cicadae fruiting bodies as an anti-inflammatory mushroom.