Your browser doesn't support javascript.
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 551
Filtrar
1.
MMWR Morb Mortal Wkly Rep ; 69(8): 201-206, 2020 Feb 28.
Artigo em Inglês | MEDLINE | ID: mdl-32106215

RESUMO

Lung cancer is the leading cause of cancer death in the United States; 148,869 lung cancer-associated deaths occurred in 2016 (1). Mortality might be reduced by identifying lung cancer at an early stage when treatment can be more effective (2). In 2013, the U.S. Preventive Services Task Force (USPSTF) recommended annual screening for lung cancer with low-dose computed tomography (CT) for adults aged 55-80 years who have a 30 pack-year* smoking history and currently smoke or have quit within the past 15 years (2).† This was a Grade B recommendation, which required health insurance plans to cover lung cancer screening as a preventive service.§ To assess the prevalence of lung cancer screening by state, CDC used Behavioral Risk Factor Surveillance System (BRFSS) data¶ collected in 2017 by 10 states.** Overall, 12.7% adults aged 55-80 years met the USPSTF criteria for lung cancer screening. Among those meeting USPSTF criteria, 12.5% reported they had received a CT scan to check for lung cancer in the last 12 months. Efforts to educate health care providers and provide decision support tools might increase recommended lung cancer screening.


Assuntos
Detecção Precoce de Câncer/estatística & dados numéricos , Neoplasias Pulmonares/prevenção & controle , Idoso , Idoso de 80 Anos ou mais , Fumar Cigarros/efeitos adversos , Fumar Cigarros/epidemiologia , Humanos , Neoplasias Pulmonares/mortalidade , Pessoa de Meia-Idade , Guias de Prática Clínica como Assunto , Abandono do Hábito de Fumar/estatística & dados numéricos , Estados Unidos/epidemiologia
2.
Food Chem Toxicol ; 135: 110930, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31678261

RESUMO

Cigarette smoke (CS) is a risk factor for the development of nonalcoholic fatty liver disease. However, the role of mainstream CS (MSCS) in the pathogenesis of nonalcoholic steatohepatitis (NASH) remains unclear. During the first (early exposure) or last (late exposure) three weeks of methionine-choline deficient with high fat diet feeding (6 weeks), each diet group was exposed to MSCS (300 or 600 µg/L). Hepatic or serum biochemical analysis showed that MSCS differentially modulated hepatic injury in NASH milieu, depending on exposure time points. Consistently, NASH-related hepatocellular apoptosis and fibrosis were increased in the early exposure group, but decreased in the late exposure group, except for steatosis. Ex vivo experiments showed that CS extract differentially regulated inflammatory responses in co-cultured hepatocytes and macrophages isolated from steatohepatitic livers after 10 days or 3 weeks of diet feeding. Furthermore, CS differentially up- and down-regulated the expression levels of M1/M2 polarization markers and peroxisome proliferator-activated receptor-gamma (PPARγ) in livers (29% and 38%, respectively) or co-cultured macrophages (2 and 2.5 fold, respectively). Collectively, our findings indicate that opposite effects of MSCS on NASH progression are mediated by differential modulation of PPARγ and its-associated M1/M2 polarization in hepatic macrophages, depending on exposure time points.


Assuntos
Fumar Cigarros/efeitos adversos , Inflamação/fisiopatologia , Hepatopatia Gordurosa não Alcoólica/fisiopatologia , Animais , Peso Corporal/efeitos dos fármacos , Deficiência de Colina , Citocinas/metabolismo , Dieta Hiperlipídica , Progressão da Doença , Inflamação/patologia , Fígado/efeitos dos fármacos , Fígado/patologia , Cirrose Hepática/patologia , Cirrose Hepática/fisiopatologia , Macrófagos/efeitos dos fármacos , Masculino , Metionina/deficiência , Camundongos Endogâmicos C57BL , Monócitos/efeitos dos fármacos , Hepatopatia Gordurosa não Alcoólica/patologia , Tamanho do Órgão/efeitos dos fármacos , PPAR gama/metabolismo , Fatores de Tempo
3.
Angiology ; 71(3): 281-287, 2020 03.
Artigo em Inglês | MEDLINE | ID: mdl-31777276

RESUMO

We sought to compare the effects of smoking on clinical outcomes in women and men with coronary artery disease undergoing percutaneous coronary intervention (PCI). We prospectively followed up 10 369 patients undergoing elective PCI. All patients were stratified according to smoking status and sex. The impacts of smoking on long-term major adverse cardiovascular events (MACEs, the composite of all-cause death, myocardial infarction, or target vessel revascularization) were assessed. Among 7773 men and 2596 women undergoing PCI, the prevalence of cigarette smoking was 66.7% (n = 5185) and 11.0% (n = 286; P < .001). During the 3 years of follow-up (median: 20.6 months), smoking increased MACE in both men and women (men 10.8% vs 8.1%, P < .001; women 23.2% vs 6.4%; P < .001). After adjusting for baseline characteristics, smoking had a greater effect on MACE in women (hazard ratio [HR]: 3.68, 95% confidence interval [CI]: 1.86-7.28; P < .001) compared with men (HR: 1.35, 95% CI: 1.03-1.77; P = .005, interaction P = .026). There was a lower prevalence of smoking in women compared to men among patients undergoing PCI. However, smoking confers a higher excess risk for MACE among women compared with men.


Assuntos
Fumar Cigarros/efeitos adversos , Doença da Artéria Coronariana/etiologia , Intervenção Coronária Percutânea , Adulto , Idoso , Angiografia Coronária/métodos , Ponte de Artéria Coronária , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Infarto do Miocárdio/etiologia , Intervenção Coronária Percutânea/efeitos adversos , Prognóstico , Modelos de Riscos Proporcionais , Fatores de Risco , Caracteres Sexuais , Resultado do Tratamento
4.
Oncology ; 98(1): 42-47, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-31437849

RESUMO

INTRODUCTION: Smoking induces inflammation and an immune response. A cancer-related inflammatory response has been seen in smoking and nonsmoking head and neck squamous cell carcinoma (HNSCC) patients. OBJECTIVES: The aim of this study was to analyze the possible separated effects of smoking or HNSCC on 18 inflammatory or immune regulatory biomarkers. METHODS: Fifty-one nonsmoking and 36 smoking pretreated HNSCC patients and 101 nonsmoking and 39 smoking controls were included in this study. The levels of 18 inflammatory or immune regulatory biomarkers were analyzed. A multivariable linear regression model was used to predict the impact of smoking and HNSCC on the levels of the biomarkers. RESULTS: Smoking had the highest impact on total WBC, IFN-γ, and MCP-1 levels. The highest impact of HNSCC was found on neutrophils, neutrophil-to-lymphocyte ratio, HsCRP, MIP-1b, and TNF-α levels. CONCLUSION: IdentifyingHNSCC or smoking-related inflammatory biomarkers might contribute to the understanding of the immune response in HNSCC patients. This study could provide information of inflammatory biomarkers in HNSCC patients.


Assuntos
Biomarcadores/sangue , Fumar Cigarros , Mediadores da Inflamação/sangue , Carcinoma de Células Escamosas de Cabeça e Pescoço/sangue , Adulto , Idoso , Idoso de 80 Anos ou mais , Estudos de Casos e Controles , Fumar Cigarros/efeitos adversos , Citocinas/metabolismo , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Estadiamento de Neoplasias , Carcinoma de Células Escamosas de Cabeça e Pescoço/diagnóstico , Carcinoma de Células Escamosas de Cabeça e Pescoço/etiologia , Carga Tumoral , Adulto Jovem
6.
Life Sci ; 241: 117132, 2020 Jan 15.
Artigo em Inglês | MEDLINE | ID: mdl-31837327

RESUMO

INTRODUCTION: This study aimed to verify the effects of cigarette smoke exposure in bone mineralization and fibrillar matrix composition as well as in bone healing after tibial fracture induction. METHODS: C57Bl/6 Mice were assigned according to exposure and surgery: C room air; F room air and tibia open osteotomy; CS cigarette smoke; FCS cigarette smoke and tibia open osteotomy. In order to study fracture healing we performed, under anesthesia, a bone injury through a tibial shaft osteotomy. Bone samples were obtained to evaluate bone histomorphometry, trabecular morphology and volume, trabecular collagen types composition and presence of inflammatory cytokines and growth factors. RESULTS: CS exposure significantly reduced the thickness of bone trabeculae associated with decrease in mineralizing surface and mineral deposition rate, leading a lower bone formation rate and longer mineralization time. Resorption surface and osteoclastic surface were greater in the CS group, attesting increased resorptive action. There was a decrease in type I collagen deposition and genes expression in the CS and FCS groups compared to C group and in contrast there was an increase in type V collagen deposition and genes expression in the CS, FC and FSC groups compared to C group. Also, CS exposure induced a decrease in bone forming cytokines and an increase in inflammatory associated cytokines, and these changes were intensified under fracture conditions. CONCLUSION: Cigarette smoke exposure alters bone matrix composition and worsens bone mineralization, leading to bone fragility by increasing collagen V synthesis and deposition and impairing collagen I fibril forming and assembling. And these deleterious effects contributed to the worsening in fracture healing after tibia osteotomy.


Assuntos
Calcificação Fisiológica/efeitos dos fármacos , Fumar Cigarros/efeitos adversos , Osteogênese/efeitos dos fármacos , Fumaça/efeitos adversos , Tíbia/patologia , Fraturas da Tíbia/patologia , Animais , Colágeno Tipo I/metabolismo , Citocinas/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Tíbia/efeitos dos fármacos , Tíbia/lesões , Tíbia/metabolismo , Fraturas da Tíbia/etiologia , Fraturas da Tíbia/metabolismo
7.
Braz Oral Res ; 33: e114, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31800865

RESUMO

This in vitro study aimed to evaluate the effect of different toothpastes on dental enamel subjected to an erosive cycle with and without exposure to cigarette smoke. Bovine enamel specimens were randomly allocated into 12 groups (n = 12). For the in vitro simulation of smoking, half the groups underwent an exposure cycle of 20 cigarettes per day for 5 days. Subsequently, all groups were subjected to a 5-day erosion cycle intercalating demineralization (1 min; 1% citric acid; pH = 3.5) and treatment with toothpaste slurries (2 min) of NaF, SnF2, F/Sn/Chitosan, F/CaSiO3/Na3PO4, and F/bioactive glass. The control group was immersed in distilled water. Surface microhardness (SMH) was measured initially, after exposure to smoke, and after the erosive cycle, and %SMH was calculated. At the end of the experimental cycle, surface roughness, profilometry, and atomic force microscopy (AFM) were performed. SMH increased after exposure to cigarette smoke (p < 0.05). After the erosive cycle, there were no differences between the presence and absence of cigarette smoke exposure in SMH and roughness (p > 0.05). Besides increasing enamel SMH, cigarette smoke did not prevent enamel loss after the erosion cycle (p < 0.05). In profilometry, roughness and surface loss had the lowest values in the groups treated with SnF2 and F/Sn/Chitosan (p < 0.05). AFM showed lower mineral loss with F/CaSiO3/Na3PO4 and F/Sn/Chitosan. For all groups, except F/CaSiO3/Na3PO4, cigarette smoke resulted in higher enamel wear. F/Sn/Chitosan showed the best results against erosion.


Assuntos
Fumar Cigarros/efeitos adversos , Esmalte Dentário/efeitos dos fármacos , Erosão Dentária/etiologia , Erosão Dentária/prevenção & controle , Cremes Dentais/uso terapêutico , Animais , Compostos de Cálcio/uso terapêutico , Cariostáticos/uso terapêutico , Bovinos , Quitosana/uso terapêutico , Testes de Dureza , Humanos , Microscopia de Força Atômica , Valores de Referência , Reprodutibilidade dos Testes , Saliva/química , Silicatos/uso terapêutico , Propriedades de Superfície/efeitos dos fármacos , Fatores de Tempo , Fluoretos de Estanho/uso terapêutico , Desmineralização do Dente/induzido quimicamente , Desmineralização do Dente/prevenção & controle , Água/química
8.
PLoS Genet ; 15(10): e1008353, 2019 10.
Artigo em Inglês | MEDLINE | ID: mdl-31671092

RESUMO

Mendelian randomization (MR) is an established approach to evaluate the effect of an exposure on an outcome. The gene-by-environment (GxE) study design can be used to determine whether the genetic instrument affects the outcome through pathways other than via the exposure of interest (horizontal pleiotropy). MR phenome-wide association studies (MR-pheWAS) search for the effects of an exposure, and can be conducted in UK Biobank using the PHESANT package. In this proof-of-principle study, we introduce the novel GxE MR-pheWAS approach, that combines MR-pheWAS with the use of GxE interactions. This method aims to identify the presence of effects of an exposure while simultaneously investigating horizontal pleiotropy. We systematically test for the presence of causal effects of smoking heaviness-stratifying on smoking status (ever versus never)-as an exemplar. If a genetic variant is associated with smoking heaviness (but not smoking initiation), and this variant affects an outcome (at least partially) via tobacco intake, we would expect the effect of the variant on the outcome to differ in ever versus never smokers. We used PHESANT to test for the presence of effects of smoking heaviness, instrumented by genetic variant rs16969968, among never and ever smokers respectively, in UK Biobank. We ranked results by the strength of interaction between ever and never smokers. We replicated previously established effects of smoking heaviness, including detrimental effects on lung function. Novel results included a detrimental effect of heavier smoking on facial aging. We have demonstrated how GxE MR-pheWAS can be used to identify potential effects of an exposure, while simultaneously assessing whether results may be biased by horizontal pleiotropy.


Assuntos
Fumar Cigarros/epidemiologia , Biologia Computacional/métodos , Análise da Randomização Mendeliana/métodos , Envelhecimento da Pele/efeitos dos fármacos , Bancos de Espécimes Biológicos , Fumar Cigarros/efeitos adversos , Fumar Cigarros/genética , Interação Gene-Ambiente , Pleiotropia Genética , Humanos , Masculino , Pessoa de Meia-Idade , Polimorfismo de Nucleotídeo Único , Estudo de Prova de Conceito , Reino Unido/epidemiologia
9.
PLoS Med ; 16(11): e1002972, 2019 11.
Artigo em Inglês | MEDLINE | ID: mdl-31721775

RESUMO

BACKGROUND: Maternal smoking during pregnancy is an established risk factor for low infant birth weight, but evidence on critical exposure windows and timing of fetal growth restriction is limited. Here we investigate the associations of maternal quitting, reducing, and continuing smoking during pregnancy with longitudinal fetal growth by triangulating evidence from 3 analytical approaches to strengthen causal inference. METHODS AND FINDINGS: We analysed data from 8,621 European liveborn singletons in 2 population-based pregnancy cohorts (the Generation R Study, the Netherlands 2002-2006 [n = 4,682]) and the Born in Bradford study, United Kingdom 2007-2010 [n = 3,939]) with fetal ultrasound and birth anthropometric measures, parental smoking during pregnancy, and maternal genetic data. Associations with trajectories of estimated fetal weight (EFW) and individual fetal parameters (head circumference, femur length [FL], and abdominal circumference [AC]) from 12-16 to 40 weeks' gestation were analysed using multilevel fractional polynomial models. We compared results from (1) confounder-adjusted multivariable analyses, (2) a Mendelian randomization (MR) analysis using maternal rs1051730 genotype as an instrument for smoking quantity and ease of quitting, and (3) a negative control analysis comparing maternal and mother's partner's smoking associations. In multivariable analyses, women who continued smoking during pregnancy had a smaller fetal size than non-smokers from early gestation (16-20 weeks) through to birth (p-value for each parameter < 0.001). Fetal size reductions in continuing smokers followed a dose-dependent pattern (compared to non-smokers, difference in mean EFW [95% CI] at 40 weeks' gestation was -144 g [-182 to -106], -215 g [-248 to -182], and -290 g [-334 to -247] for light, moderate, and heavy smoking, respectively). Overall, fetal size reductions were most pronounced for FL. The fetal growth trajectory in women who quit smoking in early pregnancy was similar to that of non-smokers, except for a shorter FL and greater AC around 36-40 weeks' gestation. In MR analyses, each genetically determined 1-cigarette-per-day increase was associated with a smaller EFW from 20 weeks' gestation to birth in smokers (p = 0.01, difference in mean EFW at 40 weeks = -45 g [95% CI -81 to -10]) and a greater EFW from 32 weeks' gestation onwards in non-smokers (p = 0.03, difference in mean EFW at 40 weeks = 26 g [95% CI 5 to 47]). There was no evidence that partner smoking was associated with fetal growth. Study limitations include measurement error due to maternal self-report of smoking and the modest sample size for MR analyses resulting in unconfounded estimates being less precise. The apparent positive association of the genetic instrument with fetal growth in non-smokers suggests that genetic pleiotropy may have masked a stronger association in smokers. CONCLUSIONS: A consistent linear dose-dependent association of maternal smoking with fetal growth was observed from the early second trimester onwards, while no major growth deficit was found in women who quit smoking early in pregnancy except for a shorter FL during late gestation. These findings reinforce the importance of smoking cessation advice in preconception and antenatal care and show that smoking reduction can lower the risk of impaired fetal growth in women who struggle to quit.


Assuntos
Peso ao Nascer/efeitos dos fármacos , Fumar Cigarros/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal/etiologia , Adulto , Feminino , Desenvolvimento Fetal , Retardo do Crescimento Fetal/etiologia , Peso Fetal , Feto , Idade Gestacional , Humanos , Recém-Nascido , Recém-Nascido Pequeno para a Idade Gestacional , Exposição Materna/efeitos adversos , Análise da Randomização Mendeliana , Países Baixos/epidemiologia , Gravidez , Primeiro Trimestre da Gravidez/efeitos dos fármacos , Estudos Prospectivos , Abandono do Hábito de Fumar/psicologia , Reino Unido/epidemiologia
10.
Curr Med Sci ; 39(5): 748-753, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31612392

RESUMO

Although several studies confirmed that berberine may attenuate airway inflammation in mice with chronic obstructive pulmonary disease (COPD), its underlying mechanisms were not clear until now. We aimed to establish an experiment mouse model for COPD and to investigate the effects of berberine on airway inflammation and its possible mechanism in COPD model mice induced by cigarette smoke extract (CSE). Twenty SPF C57BL/6 mice were randomly divided into PBS control group, COPD model group, low-dose berberine group and high-dose berberine group, 5 mice in each group. The neutrophils and macrophages were examined by Wright's staining. The levels of inflammatory cytokines TNF-α and IL-6 in bronchoalveolar lavage fluid (BALF) were determined by enzyme-linked immunosorbent assay. The expression levels of TGF-ß1, Smad2 and Smad3 mRNA and proteins in lung tissues were respectively detected by quantitative real-time polymerase chain reaction and Western blotting. It was found that CSE increased the number of inflammation cells in BALF, elevated lung inflammation scores, and enhanced the TGF-ß1/Smads signaling activity in mice. High-dose berberine restrained the alterations in the COPD mice induced by CSE. It was concluded that high-dose berberine ameliorated CSE-induced airway inflammation in COPD mice. TGF-ß1/Smads signaling pathway might be involved in the mechanism. These findings suggested a therapeutic potential of high-dose berberine on the CSE-induced airway inflammation.


Assuntos
Anti-Inflamatórios não Esteroides/farmacologia , Berberina/farmacologia , Pulmão/efeitos dos fármacos , Doença Pulmonar Obstrutiva Crônica/tratamento farmacológico , Proteína Smad2/genética , Proteína Smad3/genética , Fator de Crescimento Transformador beta1/genética , Animais , Líquido da Lavagem Broncoalveolar/química , Líquido da Lavagem Broncoalveolar/imunologia , Fumar Cigarros/efeitos adversos , Misturas Complexas/antagonistas & inibidores , Misturas Complexas/farmacologia , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Esquema de Medicação , Regulação da Expressão Gênica , Inflamação , Interleucina-6/genética , Interleucina-6/imunologia , Pulmão/imunologia , Pulmão/patologia , Macrófagos/efeitos dos fármacos , Macrófagos/imunologia , Macrófagos/patologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Neutrófilos/efeitos dos fármacos , Neutrófilos/imunologia , Neutrófilos/patologia , Doença Pulmonar Obstrutiva Crônica/genética , Doença Pulmonar Obstrutiva Crônica/imunologia , Doença Pulmonar Obstrutiva Crônica/patologia , Transdução de Sinais , Proteína Smad2/imunologia , Proteína Smad3/imunologia , Fator de Crescimento Transformador beta1/antagonistas & inibidores , Fator de Crescimento Transformador beta1/imunologia , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/imunologia
11.
Toxicol Lett ; 317: 92-101, 2019 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-31593750

RESUMO

Cigarette smoke (CS) is known to cause mitochondrial dysfunction leading to cellular senescence in lung cells. We determined the mechanism of mitochondrial dysfunction by CS in lung epithelial cells. CS extract (CSE) treatment differentially affected mitochondrial function, such as membrane potential, mitochondrial reactive oxygen species (mtROS) and mitochrondrial mass as analyzed by FACS, and were associated with altered oxidative phosphorylation (OXPHOS) protein levels (Complexes I-IV) in primary lung epithelial cells (SAEC and NHBE), and (complexes I and II) in BEAS2B cells. There were dose- and time-dependent changes in mitochondrial respiration (oxygen consumption rate parameters i.e. maximal respiration, ATP production and spare capacity, measured by the Seahorse analyzer) in control vs. CSE treated BEAS2B and NHBE/DHBE cells. Electron microscopy (EM) analysis revealed perinuclear clustering by localization and increased mitochondrial fragmentation by fragement length analysis. Immunoblot analysis revealed CS-mediated increase in Drp1 and decrease in Mfn2 levels that are involved in mitochondrial fission/fusion process. CSE treatment reduced Miro1 and Pink1 abundance that play a crucial role in the intercellular transfer mechanism and mitophagy process. Overall, these findings highlight the role of Miro1 in context of CS-induced mitochondrial dysfunction in lung epithelial cells that may contribute to the pathogenesis of chronic inflammatory lung diseases.


Assuntos
Fumar Cigarros/efeitos adversos , Células Epiteliais/metabolismo , Pulmão/metabolismo , Mitocôndrias/metabolismo , Proteínas Mitocondriais/metabolismo , Doença Pulmonar Obstrutiva Crônica/etiologia , Fumaça/efeitos adversos , Proteínas rho de Ligação ao GTP/metabolismo , Estudos de Casos e Controles , Células Cultivadas , Regulação para Baixo , Metabolismo Energético , Células Epiteliais/ultraestrutura , Humanos , Pulmão/ultraestrutura , Mitocôndrias/ultraestrutura , Estresse Oxidativo , Doença Pulmonar Obstrutiva Crônica/metabolismo , Doença Pulmonar Obstrutiva Crônica/patologia , Transdução de Sinais
12.
Drug Des Devel Ther ; 13: 3259-3268, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31571828

RESUMO

Background: Cigarette smoke (CS) results in chronic mucus hypersecretion and airway inflammation, contributing to COPD pathogenesis. Mucin 5B (MUC5B) and mucin 5 AC (MUC5AC) are major mucins implicated in COPD pathogenesis. Carbocisteine can reduce mucus viscosity and elasticity. Although carbocisteine decreased human elastase-induced MUC5AC expression in vitro and reduced MUC5AC expression that alleviated bacteria adhesion and improved mucus clearance in vivo, the roles of carbocisteine in inducing MUC5B expression in COPD remain unclear. Methods: To investigate the Muc5b/Muc5ac ratio and the gene and protein levels of Muc5b in COPD and carbocisteine intervention models. C57B6J mice were used to develop COPD model by instilling intratracheally with lipopolysaccharide on days 1 and 14 and were exposed to CS for 2 hr twice a day for 12 weeks. Low and high doses of carbocisteine 112.5 and 225 mg/kg/d, respectively, given by gavage administration were applied for the treatment in COPD models for the same duration, and carboxymethylcellulose was used as control. Carbocisteine significantly attenuated inflammation in bronchoalveolar lavage fluid and pulmonary tissue, improved pulmonary function and protected against emphysema. Results: High-dose carbocisteine significantly decreased the overproduction of Muc5b (P<0.01) and Muc5ac (P<0.001), and restored Muc5b/Muc5ac ratio in COPD model group (P<0.001). Moreover, the Muc5b/Muc5ac ratio negatively correlated with pro-inflammatory cytokines such as IL-6 and keratinocyte-derived cytokine, mean linear intercept, functional residual capacity and airway resistance, but positively correlated with dynamic compliance. Conclusions: These findings suggest that carbocisteine attenuated Muc5b and Muc5ac secretion and restored Muc5b protein levels, which may improve mucus clearance in COPD.


Assuntos
Carbocisteína/uso terapêutico , Mucina-5AC/metabolismo , Mucina-5B/metabolismo , Doença Pulmonar Obstrutiva Crônica/tratamento farmacológico , Animais , Quimiocinas/metabolismo , Fumar Cigarros/efeitos adversos , Modelos Animais de Doenças , Enfisema/prevenção & controle , Inflamação/tratamento farmacológico , Inflamação/metabolismo , Interleucina-6/metabolismo , Lipopolissacarídeos/administração & dosagem , Pulmão/imunologia , Pulmão/metabolismo , Pulmão/patologia , Camundongos , Muco/metabolismo , Doença Pulmonar Obstrutiva Crônica/imunologia
13.
Toxicol Lett ; 317: 102-109, 2019 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-31574306

RESUMO

BACKGROUND: Cigarette smoke is considered a risk factor for lung and colorectal cancer. A convincing link between epithelial-to-mesenchymal transition (EMT) with colorectal cancer progression and therapeutic resistance has emerged. Deregulated expression of E-Cadherin and Claudin-1 and increased miR-21 expression and invasiveness represent hallmarks of EMT. The effects of cigarette smoke exposure on EMT in colorectal adenocarcinoma cells are largely unknown. AIM: The aim of the study is to evaluate the effect of cigarette smoke extract (CSE) on miR-21, Claudin-1 and E-Cadherin, molecules associated to EMT in colorectal cancer cells. METHODS: A human colorectal adenocarcinoma cell line (Caco-2) was treated with CSE at different concentration (5% and 10%) and for different time points (3 h and 24 h). Metabolic activity (by MTS assay), cell necrosis/cell apoptosis (evaluating Propidium Iodide/Annexin V expression by flow cytometry), miR-21, Claudin-1 and E-Cadherin gene expression were evaluated by Real time PCR. Cell permeability, actin polymerization and cancer cell migration was assessed by Trans-Epitelial Electrical Resistance (TEER), Phalloidin expression and matrigel system, respectively. RESULTS: CSE at all the tested concentrations and at all time points reduced cell necrosis. CSE at 10% increased miR-21 and reduced the metabolic activity, cell necrosis, Claudin-1 and E-cadherin mRNA at 3 h. Cell permeability, actin polymerization and cancer cell migration were all increased upon CSE exposure. CONCLUSION: These results showed that CSE increasing miR-21, Claudin-1 and E-Cadherin and enhancing the aggressiveness of cancer cells, may concur to colorectal cancer progression.


Assuntos
Adenocarcinoma/metabolismo , Antígenos CD/metabolismo , Caderinas/metabolismo , Movimento Celular , Fumar Cigarros/efeitos adversos , Claudina-1/metabolismo , Neoplasias Colorretais/metabolismo , MicroRNAs/metabolismo , Fumaça/efeitos adversos , Adenocarcinoma/genética , Adenocarcinoma/patologia , Antígenos CD/genética , Células CACO-2 , Caderinas/genética , Claudina-1/genética , Neoplasias Colorretais/genética , Neoplasias Colorretais/patologia , Progressão da Doença , Transição Epitelial-Mesenquimal , Regulação Neoplásica da Expressão Gênica , Humanos , MicroRNAs/genética , Invasividade Neoplásica , Transdução de Sinais
14.
Pol J Pathol ; 70(1): 21-25, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31556547

RESUMO

Our understanding of aetiological factors associated with urinary bladder cancer has radically improved over the last decades. Cigarette smoking is considered the most important risk factor, even in the industrialised world, while various occupational and environmental exposures to chemicals are also held responsible. The link between bladder cancer and schistosomiasis, highly prevalent in sub-Saharan Africa, Sudan, Egypt, and Yemen, provides input for investigating and potentially preventing bladder carcinogenesis. Growing concern regarding environmental diseases prompts investigation into the historical milestones that have helped disentangle the relationships between health and environment.


Assuntos
Fumar Cigarros/efeitos adversos , Exposição Ambiental/efeitos adversos , Esquistossomose/complicações , Neoplasias da Bexiga Urinária/complicações , Neoplasias da Bexiga Urinária/etiologia , Humanos , Fatores de Risco
15.
Pol J Pathol ; 70(2): 134-138, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31556564

RESUMO

Smoking has a damaging effect on the musculoskeletal system, which was presented by authors in the rotator cuff and Achilles tendons studies; however, there are a lack of data about the effect of smoking on disorders of the long head of the biceps tendon (LHBT), particularly at the microscopic level. The purpose of this study was to investigate the effect of the tobacco smoking on the histopathologic alterations of the LHBT. Thirty-six patients with preoperatively diagnosed tendinopathy of the LHBT were referred to the Orthopaedics Department. All patients underwent arthroscopic treatment with further macroscopic and microscopic evaluation of biceps tendon samples. The active and former smokers were characterised by more advanced degenerative process of the tendinous tissue; moreover, it was intensified in the group of former smokers. Subjects who smoke more than 20 cigarettes per day also had more advanced microscopic alterations. The most severe microscopic alterations occurred in the former smokers who used tobacco for more than 20 years. However, the non-smokers group revealed moderate degeneration in all LHBT samples. Tobacco smoking is an important risk factor of the LHBT disease, which essentially intensifies the degeneration of the tendinous tissue.


Assuntos
Fumar Cigarros/efeitos adversos , Tendinopatia/patologia , Tendões/patologia , Artroscopia , Humanos
16.
Acta Diabetol ; 56(12): 1315-1321, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31493030

RESUMO

AIM: To assess the association between alcohol consumption and/or cigarette smoking with other unhealthy behaviors and clinical cardiovascular risk factors in youth with type 1 diabetes. METHODS: Two hundred and twenty-eight youth with type 1 diabetes (age 13-19 years) were consecutively enrolled in three Regional Pediatric Diabetes Centers in Italy. Demographic, anthropometric, lifestyle (adherence to the Mediterranean diet pattern and sports participation) and laboratory parameters were compared among youth reporting isolated or combined alcohol consumption and/or cigarette smoking. RESULTS: Ten percent of the youth reported alcohol consumption, 10% cigarette smoking and 6% both alcohol and cigarette use; 74% did not report alcohol or cigarette use. Compared to non-drinker non-smoker youth, smokers showed significantly higher percentages of each of the behavioral and clinical cardiovascular risk factors. Drinkers showed a significantly higher proportion of abdominal adiposity, dyslipidemia and poor adherence to the Mediterranean diet. Alcohol consumption was independently associated with both dyslipidemia and high glycosylated hemoglobin. CONCLUSIONS: Our findings emphasize the need to increase the awareness of youth with T1D about the negative impact of alcohol drinking on cardiovascular risk, since the effects of alcohol might be underestimated with respect to the well-known detrimental effects of smoking. Clustering of unhealthy lifestyle should be discouraged in type 1 diabetes youth in order to promote cardiovascular protection.


Assuntos
Consumo de Bebidas Alcoólicas/epidemiologia , Doenças Cardiovasculares/epidemiologia , Fumar Cigarros/epidemiologia , Diabetes Mellitus Tipo 1/epidemiologia , Angiopatias Diabéticas/epidemiologia , Adolescente , Adulto , Consumo de Bebidas Alcoólicas/efeitos adversos , Doenças Cardiovasculares/etiologia , Fumar Cigarros/efeitos adversos , Diabetes Mellitus Tipo 1/sangue , Diabetes Mellitus Tipo 1/complicações , Angiopatias Diabéticas/etiologia , Feminino , Hemoglobina A Glicada/análise , Hemoglobina A Glicada/metabolismo , Humanos , Itália/epidemiologia , Estilo de Vida , Masculino , Fatores de Risco , Fumar/efeitos adversos , Fumar/epidemiologia , Adulto Jovem
17.
J Korean Med Sci ; 34(31): e213, 2019 Aug 12.
Artigo em Inglês | MEDLINE | ID: mdl-31392856

RESUMO

BACKGROUND: Tobacco smoking affects the incidence of various illnesses such as lung cancer, respiratory diseases, and cardiovascular diseases. In an effort to prevent smoking-related cancers, we aimed to estimate the smoking prevalence, intensity, and number of workers exposed to smoking, which would be specific to the occupational and industrial circumstances in Korea. METHODS: We used the Korean Working Condition Survey (KWCS) and Korea's Census data. Smoking prevalence and intensity were estimated using the KWCS data. The number of smokers was estimated by multiplying smoking prevalence with the number of workers in the occupation or industry. Smoking prevalence, intensity, and number of smokers were estimated for major, sub-major, and minor groups of occupation and industry. RESULTS: Of the total labor force in 2010, 52.66% of men and 5.24% of women workers were estimated to be current smokers. Men workers smoked 15.42 cigarettes/day, and women workers 11.29 cigarettes/day. In terms of occupation, "craft and related trades workers" demonstrated the highest smoking prevalence (52.24%). "Managers" smoked the highest number of cigarettes (16.63 cigarettes/day) and "equipment, machine operating, and assembling workers" comprised the largest number of estimated smokers (1,368,726 workers). In terms of industry, "mining and quarrying" had the highest smoking prevalence (69.27%). Those in "construction" smoked the highest number of cigarettes (17.16 cigarettes/day) and those in "manufacturing" comprised the largest number of estimated smokers (1,629,893 workers). CONCLUSION: Our results may help in setting priorities for smoking prevention-related activities. In addition, these results can be used for epidemiological studies controlling for the effect of smoking by occupation or industry.


Assuntos
Fumar Cigarros/efeitos adversos , Inquéritos Epidemiológicos , Doenças Profissionais/epidemiologia , Exposição Ocupacional , Poluição por Fumaça de Tabaco/efeitos adversos , Adolescente , Adulto , Idoso , Emprego/estatística & dados numéricos , Feminino , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Saúde do Trabalhador , Ocupações , Prevalência , República da Coreia/epidemiologia , Risco , Fumantes , Fumar , Adulto Jovem
18.
Respir Res ; 20(1): 181, 2019 Aug 09.
Artigo em Inglês | MEDLINE | ID: mdl-31399087

RESUMO

BACKGROUND: KRAS is a GTPase that activates pathways involved in cell growth, differentiation and survival. In normal cells, KRAS-activity is tightly controlled, but with specific mutations, the KRAS protein is persistently activated, giving cells a growth advantage resulting in cancer. While a great deal of attention has been focused on the role of mutated KRAS as a common driver mutation for lung adenocarcinoma, little is known about the role of KRAS in regulating normal human airway differentiation. METHODS: To assess the role of KRAS signaling in regulating differentiation of the human airway epithelium, primary human airway basal stem/progenitor cells (BC) from nonsmokers were cultured on air-liquid interface (ALI) cultures to mimic the airway epithelium in vitro. Modulation of KRAS signaling was achieved using siRNA-mediated knockdown of KRAS or lentivirus-mediated over-expression of wild-type KRAS or the constitutively active G12 V mutant. The impact on differentiation was quantified using TaqMan quantitative PCR, immunofluorescent and immunohistochemical staining analysis for cell type specific markers. Finally, the impact of cigarette smoke exposure on KRAS and RAS protein family activity in the airway epithelium was assessed in vitro and in vivo. RESULTS: siRNA-mediated knockdown of KRAS decreased differentiation of BC into secretory and ciliated cells with a corresponding shift toward squamous cell differentiation. Conversely, activation of KRAS signaling via lentivirus mediated over-expression of the constitutively active G12 V KRAS mutant had the opposite effect, resulting in increased secretory and ciliated cell differentiation and decreased squamous cell differentiation. Exposure of BC to cigarette smoke extract increased KRAS and RAS protein family activation in vitro. Consistent with these observations, airway epithelium brushed from healthy smokers had elevated RAS activation compared to nonsmokers. CONCLUSIONS: Together, these data suggest that KRAS-dependent signaling plays an important role in regulating the balance of secretory, ciliated and squamous cell differentiation of the human airway epithelium and that cigarette smoking-induced airway epithelial remodeling is mediated in part by abnormal activation of KRAS-dependent signaling mechanisms.


Assuntos
Diferenciação Celular/fisiologia , Fumar Cigarros/efeitos adversos , Fumar Cigarros/metabolismo , Proteínas Proto-Oncogênicas p21(ras)/fisiologia , Mucosa Respiratória/metabolismo , Poluição por Fumaça de Tabaco/efeitos adversos , Adulto , Remodelação das Vias Aéreas/efeitos dos fármacos , Remodelação das Vias Aéreas/fisiologia , Diferenciação Celular/efeitos dos fármacos , Células Cultivadas , Fumar Cigarros/patologia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Mucosa Respiratória/efeitos dos fármacos , Mucosa Respiratória/patologia , Adulto Jovem
19.
Crit Rev Oncol Hematol ; 142: 86-93, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31387065

RESUMO

PURPOSE: We aim to provide the most accurate and updated quantification of the effect of cigarette smoking on kidney cancer risk focusing on dose-response relationships. METHODS: We conducted a meta-analysis, using an innovative approach combining an umbrella review and a traditional literature search. RESULTS: Fifty-six original studies were included, providing pooled relative risks (RR) of kidney cancer of 1.39 (95% confidence interval, CI: 1.28-1.51) for current and 1.20 (95% CI: 1.14-1.27) for former compared with never smokers. Kidney cancer risk increased non-linearly with smoking intensity, the RR compared with never smokers being 1.18 (95% CI: 1.11-1.26) for five and 1.72 (95% CI: 1.52-1.95) for 30 cigarettes/day, and increased linearly with smoking duration, the RR being 1.70 (95% CI: 1.10-2.64) after 25 years. The risk linearly decreased with time-since-quitting. CONCLUSIONS: Even smoking few cigarettes per day significantly increases kidney cancer risk. Quitting smoking reduces the risk, the earlier the better.


Assuntos
Fumar Cigarros/efeitos adversos , Neoplasias Renais/etiologia , Carcinoma de Células Renais/epidemiologia , Carcinoma de Células Renais/etiologia , Relação Dose-Resposta a Droga , Feminino , Humanos , Neoplasias Renais/epidemiologia , Masculino , Fatores de Risco
20.
Med Sci Monit ; 25: 6104-6109, 2019 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-31414668

RESUMO

BACKGROUND Smoking may be a risk factor for marginal bone loss (MBL) and oral mucosal inflammation surrounding dental implants. This retrospective study evaluated the effects of smoking on dental implants in patients with fixed implant-supported prostheses over a period of 36 months following loading. MATERIAL AND METHODS We assessed 120 patients (68 women, 52 men, ages 19-74 years (mean age: 55.10 years) with 315 implants. Implants were classified according to location in the upper and lower jaws and anterior (placed between canines) or posterior (placed between pre-molars and molars) as follows: 1=maxilla anterior, 2=maxilla posterior, 3=mandible anterior, 4=mandible posterior. We also measured MBL, plaque index (PI), sulcus bleeding index (SBI), and probing depth (PD). P-values less than 0.05 were considered statistically significant. RESULTS MBL was statistically greater in smokers (P<0.001) as compared to non-smokers in both jaws. MBL did not vary significantly by location in either group (smokers: p=0.415; non-smokers: p=0.175). Mean PI and PD scores were significantly higher in smokers as compared to non-smokers (P<0.001). A positive correlation was found between PI and PD scores in both groups. No statistically significant difference in SBI was observed between the 2 groups (P>0.05). CONCLUSIONS Smoking was associated with increases in marginal bone loss around implants, independent of their location in the jaws. Also, both plaque indices and probing depths were greater in smokers than in non-smokers.


Assuntos
Perda do Osso Alveolar/etiologia , Fumar Cigarros/efeitos adversos , Adulto , Idoso , Perda do Osso Alveolar/metabolismo , Implantes Dentários , Índice de Placa Dentária , Prótese Dentária Fixada por Implante , Feminino , Seguimentos , Humanos , Masculino , Mandíbula , Doenças Mandibulares/etiologia , Pessoa de Meia-Idade , Índice Periodontal , Estudos Retrospectivos , Fumantes
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA