Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 46.163
Filtrar
Mais filtros











Intervalo de ano de publicação
1.
Zhong Nan Da Xue Xue Bao Yi Xue Ban ; 47(3): 334-343, 2022 Mar 28.
Artigo em Inglês, Chinês | MEDLINE | ID: mdl-35545326

RESUMO

OBJECTIVES: Pulmonary Langerhans cell histiocytosis (PLCH) is a clonal disease, characterized by proliferation of Langerhans cells that derived from bone marrow infiltrating the lungs and other organs. Due to the rarity of the disease, the current understanding of the disease is insufficient, often misdiagnosed or missed diagnosis. This study aims to raise clinicians' awareness for this disease via summarizing the clinical characteristics, imaging features, and treatment of PLCH. METHODS: We retrospectively analyzed clinical and follow-up data of 15 hospitalized cases of PLCH from September 2012 to June 2021 in the Second Xiangya Hospital of Central South University. RESULTS: The age of 15 patients (9 men and 6 women, with a sex ratio of 3 to 2) was 21-52 (median 33) years. Among them, 8 had a history of smoking and 5 suffered spontaneous pneumothorax during disease course. There were 3 patients with single system PLCH and 12 patients with multi-system PLCH, including 7 patients with pituitary involvement, 7 patients with lymph node involvement, 6 patients with bone involvement, 5 patients with liver involvement, 2 patients with skin involvement, 2 patients with thyroid involvement, and 1 patients with thymus involvement. The clinical manifestations were varied but non-specific. Respiratory symptoms mainly included dry cough, sputum expectoration, chest pain, etc. Constitutional symptoms included fever and weight loss. Patients with multi-system involvement experienced symptoms such as polyuria-polydipsia, bone pain, and skin rash. All patients were confirmed by pathology, including 6 by lung biopsy, 3 by bone biopsy, 2 by lymph node biopsy, and 4 by liver, skin, suprasternal fossa tumor, or pituitary stalk biopsy. The most common CT findings from this cohort of patients were nodules and/or cysts and nodular and cystic shadows were found in 7 patients. Three patients presented simple multiple cystic shadows, 3 patients presented multiple nodules, and 2 patients presented with single nodules and mass shadows. Pulmonary function tests were performed in 4 patients, ventilation dysfunction was showed in 2 patients at the first visit. Pulmonary diffusion function tests were performed in 4 patients and showed a decrease in 3 patients. Smoking cessation was recommended to PLCH patients with smoking history. Ten patients received chemotherapy while 2 patients received oral glucocorticoid therapy. Among the 11 patients with the long-term follow-up, 9 were in stable condition. CONCLUSIONS: PLCH is a neoplastic disease closely related to smoking. The clinical manifestations and laboratory examination are not specific. Pneumothorax could be the first symptom which is very suggestive of the disease. Definitive diagnosis relies on histology. There is no unified treatment plan for PLCH, and individualized treatment should be carried out according to organ involvement. Early smoking cessation is essential. Chemotherapy is the main treatment for rapidly progressing PLCH involved multiple organs. All diagnosed patients can be considered for the detection of BRAFV600E gene and relevant targeted therapies have been implemented recently.


Assuntos
Cistos , Histiocitose de Células de Langerhans , Abandono do Hábito de Fumar , Adulto , Feminino , Histiocitose de Células de Langerhans/diagnóstico , Histiocitose de Células de Langerhans/patologia , Histiocitose de Células de Langerhans/terapia , Humanos , Pulmão/patologia , Masculino , Estudos Retrospectivos , Fumar/efeitos adversos
2.
Comput Math Methods Med ; 2022: 7169353, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35529255

RESUMO

The prevalence of lung cancer induced by cigarette smoking has increased over time. Long noncoding (lnc) RNAs, regulatory factors that play a role in human diseases, are commonly dysregulated in lung cancer. Cigarette smoking is closely related to changes in lncRNA expression, which can affect lung cancer. Herein, we assess the mechanism of lung cancer initiation induced by smoking. To calculate the impact of smoking on the survival of patients with lung cancer, we extracted data from The Cancer Genome Atlas and Gene Expression Omnibus databases and identified the differentially expressed genes in the lung cancer tissue compared to the normal lung tissue. Genes positively and negatively associated with smoking were identified. Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and Cytoscape analyses were performed to determine the function of the genes and the effects of smoking on the immune microenvironment. lncRNAs corresponding to smoking-associated genes were identified, and a smoking-related lncRNA model was constructed using univariate and multivariate Cox analyses. This model was used to assess the survival of and potential risk in patients who smoked. During screening, 562 differentially expressed genes were identified, and we elucidated that smoking affected the survival of patients 4.5 years after the diagnosis of lung cancer. Furthermore, genes negatively associated with smoking were closely associated with immunity. Twelve immune cell types were also found to infiltrate differentially in smokers and nonsmokers. Thus, the smoking-associated lncRNA model is a good predictor of survival and risk in smokers and may be used as an independent prognostic factor for lung cancer.


Assuntos
Neoplasias Pulmonares , RNA Longo não Codificante , Biomarcadores Tumorais/genética , Biomarcadores Tumorais/metabolismo , Regulação Neoplásica da Expressão Gênica , Redes Reguladoras de Genes , Humanos , Neoplasias Pulmonares/genética , Prognóstico , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Fumar/efeitos adversos , Microambiente Tumoral
3.
Sci Rep ; 12(1): 7248, 2022 May 04.
Artigo em Inglês | MEDLINE | ID: mdl-35508625

RESUMO

Clonal hematopoiesis of indeterminate potential (CHIP) and mosaic chromosomal alterations (mCAs) represent two forms of clonal hematopoiesis where clones bearing expanded somatic mutations have been linked to both oncologic and non-oncologic clinical outcomes including atherosclerosis and all-cause mortality. Epidemiologic studies have highlighted smoking as an important driver of somatic mutations across multiple tissues. However, establishing the causal role of smoking in clonal hematopoiesis has been limited by observational study designs, which may suffer from confounding and reverse-causality. We performed two complementary analyses to investigate the role of smoking in mCAs and CHIP. First, using an observational study design among UK Biobank participants, we confirmed strong associations between smoking and mCAs. Second, using two-sample Mendelian randomization, smoking was strongly associated with mCA but not with CHIP. Overall, these results support a causal association between smoking and mCAs and suggest smoking may variably shape the fitness of clones bearing somatic mutations.


Assuntos
Aterosclerose , Hematopoiese Clonal , Aterosclerose/genética , Aberrações Cromossômicas , Hematopoiese Clonal/genética , Hematopoese/genética , Humanos , Mutação , Fumar/efeitos adversos , Fumar/genética
4.
Sci Rep ; 12(1): 7659, 2022 May 10.
Artigo em Inglês | MEDLINE | ID: mdl-35538134

RESUMO

We aimed to investigate the causality between potentially modifiable risk factors and the risk of intracranial aneurysm. Genetic instruments for 51 modifiable factors and intracranial aneurysm data were obtained from recently published genome-wide association studies. We applied two-sample Mendelian randomization methods to investigate their causal relationships. Genetically predicted cigarettes per day, smoking initiation, systolic blood pressure, hypertension and body fat percentage were significantly associated with an increased risk of intracranial aneurysm [odds ratios (OR) 2.67, 95% confidence interval (CI) 1.75-4.07, p = 5.36 × 10-6, OR 1.53, 95% CI 1.32-1.77, p = 9.58 × 10-9, OR 1.05, 95% CI 1.02-1.08, p = 1.18 × 10-3, OR 1.65, 95% CI 1.19-2.28, p = 2.56 × 10-3 and OR 1.29, 95% CI 1.11-1.52, p = 1.33 × 10-3, respectively]. Type 2 diabetes mellitus was significantly associated with a decreased risk of intracranial aneurysm (OR 0.89, 95% CI 0.83-0.95, p = 8.54 × 10-4). Body fat percentage was significantly associated with subarachnoid haemorrhage (p = 5.70 × 10-5). This study provided genetic evidence of causal effects of smoking, blood pressure, type 2 diabetes mellitus and obesity on the risk of intracranial aneurysm.


Assuntos
Diabetes Mellitus Tipo 2 , Aneurisma Intracraniano , Estudo de Associação Genômica Ampla , Humanos , Aneurisma Intracraniano/epidemiologia , Aneurisma Intracraniano/genética , Análise da Randomização Mendeliana , Polimorfismo de Nucleotídeo Único , Fatores de Risco , Fumar/efeitos adversos
5.
Sci Rep ; 12(1): 7665, 2022 May 10.
Artigo em Inglês | MEDLINE | ID: mdl-35538186

RESUMO

Smoking influences the risks of inflammatory bowel disease (IBD). A hospital-based cohort was conducted to evaluate the effect of smoking on the development and outcomes of IBD, with age, sex and comorbidities matched non-IBD controls from the National Health Interview Survey database of Taiwan. 700 IBD patients (360 ulcerative colitis (UC), 340 Crohn's disease (CD)) were analyzed for outcomes; and 575 patients (297 UC, 278 CD) were analyzed for prevalence. Smoking prevalence was significantly lower in UC patients than controls (20.9% vs. 30.4%, p < 0.01), but no difference between CD patients and controls (19.8% vs. 22.1%, p = 0.60). UC smokers had fewer admissions (1.6 vs. 2.5, p < 0.05) but higher rates of new cancer development (16% vs. 6.7%, p < 0.05) and mortality (16% vs. 4.9%, p < 0.01) than nonsmokers. CD smokers tended to have higher rates of stricturing and penetrating diseases (p < 0.05), and higher surgery risk (60.3% vs. 38.3%, p < 0.01) than nonsmokers. Smoking prevents UC occurrence and is associated with fewer hospitalization but increases risks of cancer and mortality. By contrast, smoking does not affect CD occurrence but is related to more aggressive behavior which results in a higher surgical rate.


Assuntos
Colite Ulcerativa , Doença de Crohn , Doenças Inflamatórias Intestinais , Neoplasias , Doença Crônica , Estudos de Coortes , Colite Ulcerativa/epidemiologia , Colite Ulcerativa/etiologia , Doença de Crohn/epidemiologia , Doença de Crohn/etiologia , Hospitais , Humanos , Doenças Inflamatórias Intestinais/epidemiologia , Doenças Inflamatórias Intestinais/etiologia , Fatores de Risco , Fumar/efeitos adversos , Fumar/epidemiologia , Taiwan/epidemiologia
6.
JNCI Cancer Spectr ; 6(2)2022 Mar 02.
Artigo em Inglês | MEDLINE | ID: mdl-35603851

RESUMO

Human papillomavirus (HPV)-associated cancer burden is rising in the United States. Trends in the incidence by county-level income and smoking prevalence remain undescribed. We used the Surveillance, Epidemiology, and End Results 21 database to ascertain HPV-associated cancers during 2000-2018. Trends were estimated by county-level income and smoking prevalence quartiles. Anal and vulvar cancer incidence among women and anal cancer incidence among men increased markedly in the lowest-income counties, whereas the increases were slower in the highest-income counties (eg, for vulvar cancer, incidence increased 1.9% per year, 95% confidence interval [CI] = 0.9% to 2.9%, in the lowest-income counties vs 0.8% per year, 95% CI = 0.6% to 1.1%, in the highest-income counties). In recent years, cervical cancer incidence plateaued (0.0% per year [95% CI = -0.5% to 0.5%]) in the highest-income counties; in the lowest-income counties, the annual percentage change was 1.6% per year (95% CI = -0.7% to 4.0%). Counties with high smoking prevalence had marked increases in incidence compared with their counterparts (eg, anal cancer among men increased 4.4% per year [95% CI = 2.7% to 6.0%] for those living in counties with the highest smoking prevalence vs 1.2% per year [95% CI = 0.7% to 1.7%] for those living in counties with the lowest smoking prevalence). Improved and targeted prevention is needed to combat the widening disparities.


Assuntos
Alphapapillomavirus , Neoplasias do Ânus , Infecções por Papillomavirus , Neoplasias Vulvares , Neoplasias do Ânus/epidemiologia , Feminino , Humanos , Incidência , Masculino , Papillomaviridae , Infecções por Papillomavirus/epidemiologia , Prevalência , Fumar/efeitos adversos , Estados Unidos/epidemiologia , Neoplasias Vulvares/epidemiologia
7.
Ann Med ; 54(1): 1385-1394, 2022 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-35576130

RESUMO

BACKGROUND: Longitudinal data on the association between smoking and glycemic control in men with newly diagnosed type 2 diabetes (T2DM) is scarce. Therefore, this study aimed to examine the extent of the association between smoking and glycemic control in this population. METHODS: The retrospective cohort study identified 3044 eligible men with T2DM in a medical centre in Taiwan between 2002 and 2017. Smokers (n = 757) were matched 1:1 with non-smokers using propensity score-matching. All of them were followed for one year. Glycated haemoglobin (HbA1c) levels were measured at 0, 3, 6, 9, and 12 months after enrolment. Generalised estimating equations were used to assess smoking status-by-time interaction to determine the difference in HbA1c reduction between the two cohorts. All analyses were performed in 2020. RESULTS: The estimated maximal difference in HbA1c reduction between smokers and non-smokers was 0.33% (95% CI, 0.05-0.62%) at 3 months of follow-up. For patients with body mass index (BMI) <25 kg/m2, the difference in HbA1c reduction between smokers and non-smokers was much larger (0.74%, 95% CI, 0.35-1.14%) than in those with a higher BMI. CONCLUSIONS: Our findings show that smoking was independently associated with unfavourable glycemic control among men with newly diagnosed T2DM, and such a detrimental association could be stronger in men with a lower BMI.


Assuntos
Diabetes Mellitus Tipo 2 , Controle Glicêmico , Glicemia/análise , Estudos de Coortes , Diabetes Mellitus Tipo 2/complicações , Diabetes Mellitus Tipo 2/epidemiologia , Hemoglobina A Glicada/análise , Humanos , Masculino , Estudos Retrospectivos , Fumar/efeitos adversos , Fumar/epidemiologia
8.
In Vivo ; 36(3): 1297-1301, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35478154

RESUMO

BACKGROUND/AIM: The prognostic role of smoking pack years after thoracic irradiation for lung cancer needs further clarification, since previous studies showed conflicting results. Therefore, this study investigated potential prognostic factors for survival including pack years in 170 lung cancer patients receiving local radiotherapy. PATIENTS AND METHODS: Twelve factors were retrospectively evaluated for survival including age, sex, tumor site, histology, primary tumor stage, nodal stage, distant metastasis, radiation dose, upfront surgery or systemic treatment, pulmonary function, and number of pack years. RESULTS: On univariate analyses, absence of distant metastasis (p=0.049), radiation dose >56 Gy (p=0.019), and ≤40 pack years (p=0.005) were significantly associated with better survival. In the multivariate analysis, number of pack years (hazard ratio 2.18, 95% confidence interval 1.25-3.82, p=0.006) maintained significance; distant metastasis (p=0.34) and radiation dose (p=0.16) were not significant. CONCLUSION: Number of pack years was an independent predictor of survival after thoracic irradiation for lung cancer.


Assuntos
Neoplasias Pulmonares , Humanos , Neoplasias Pulmonares/tratamento farmacológico , Estadiamento de Neoplasias , Prognóstico , Estudos Retrospectivos , Fumar/efeitos adversos
9.
Cancer Epidemiol ; 78: 102162, 2022 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-35461154

RESUMO

BACKGROUND: Smoking is well known to be a major risk factor for cancer, and to decrease the levels of aryl hydrocarbon receptor repressor (AHRR) DNA methylation. AHRR is a key regulator for AHR signaling, which is involved in chemical metabolism and cancer development. Therefore, smoking-induced AHRR DNA hypomethylation may be associated with cancer development. However, it has not been reported that association between AHHR DNA methylation and cancer mortality in Asian population. Hence, we examined whether AHRR DNA methylation levels were associated with cancer mortality in a Japanese population. METHODS: This study was conducted with 812 participants (aged 38-80 years) who received a health check-up in 1990, and did not have a clinical histories. We followed up the participants until the end of 2019 (median: 27.8 years), and 100 participants died from cancer. The AHRR DNA methylation levels in peripheral blood mononuclear cells (PBMCs) were measured by the pyrosequencing method. We calculated the hazard ratio (HR) and 95% confidence interval (CI) for cancer mortality according to the baseline levels of AHRR DNA methylation. RESULTS: We found that AHRR DNA hypomethylation was associated with a higher risk of all cancer mortality, especially smoking related cancers and lung cancer. (all cancer: HR, 1.28, 95% CI, 1.09-1.51; smoking-related cancers: HR, 1.35, 95% CI, 1.12-1.62; lung cancer: HR, 1.68, 95% CI, 1.24-2.26). CONCLUSIONS: Smoking-induced AHRR DNA hypomethylation in PBMCs was associated with the risk of cancer mortality in Japanese population; therefore, hypomethylation of AHRR may be a useful biomarker of cancer mortality risk.


Assuntos
Metilação de DNA , Neoplasias Pulmonares , Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética , Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo , Estudos de Coortes , DNA/metabolismo , Humanos , Japão/epidemiologia , Leucócitos Mononucleares/metabolismo , Neoplasias Pulmonares/epidemiologia , Receptores de Hidrocarboneto Arílico/genética , Receptores de Hidrocarboneto Arílico/metabolismo , Proteínas Repressoras/genética , Proteínas Repressoras/metabolismo , Fumar/efeitos adversos
10.
Biomed Khim ; 68(2): 134-143, 2022 Apr.
Artigo em Russo | MEDLINE | ID: mdl-35485487

RESUMO

To date, there are no drugs that can prevent progressive destruction of lung tissue and small airway fibrosis in patients with chronic obstructive pulmonary disease (COPD). Therefore, molecular mechanisms of this disease are being studied. The aim of this study was to determine the chemokine receptor expression pattern of B-lymphocytes from peripheral blood and airways of patients with COPD. Peripheral blood was collected from 51 smokers with COPD, 21 healthy smokers, and 20 healthy non-smokers. Seven smokers with COPD and 7 healthy smokers were recruited to undergo bronchoscopy with bronchoalveolar lavage (BAL). The expression of chemokine receptors CCR5, CCR6, CCR7, CXCR3, CXCR4, and CXCR5 on the surface of blood and BAL B-lymphocytes was determined by flow cytometry. It was found that the percentage of blood B-lymphocytes expressing chemokine receptors CCR5 and CXCR3 was higher in smokers with COPD compared with healthy smokers and healthy non-smokers. The percentage of CD27⁺ B-cells expressing CCR5 and CXCR3 receptors exceeded the proportion of CD27⁻ B-lymphocytes expressing these receptors in peripheral blood of patients with COPD and healthy controls. In smoking patients with COPD, the percentage of BAL B-cells expressing receptors CCR5 and CXCR3 was also increased compared with healthy smokers. There were no differences in the percentage of B-lymphocytes expressing receptors CXCR4, CXCR5, CCR6, and CCR7 in both peripheral blood and BAL between smokers with COPD and healthy smokers. A greater percentage of CD27⁻ B-lymphocytes than CD27⁺ B-cells expressed receptors CXCR4, CXCR5, CCR6, and CCR7 in the peripheral blood of smokers with COPD and healthy controls. The results of this study indicate a modification in the chemokine receptor profile of B-lymphocytes in COPD.


Assuntos
Doença Pulmonar Obstrutiva Crônica , Linfócitos B/metabolismo , Humanos , Pulmão/metabolismo , Doença Pulmonar Obstrutiva Crônica/genética , Receptores CCR7/metabolismo , Fumar/efeitos adversos , Fumar/metabolismo
11.
Asian Pac J Cancer Prev ; 23(4): 1199-1206, 2022 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-35485676

RESUMO

OBJECTIVE: This study aims to examine the joint effect of H. pylori infection and tobacco smoking on the development of stomach cancer among Vietnamese men. METHODS: A total of 80 stomach cancer cases and 146 controls were recruited in a case-control study conducted in a general hospital. Information on sociodemographic, anthropometric characteristics, tobacco smoking, and the dietary pattern was obtained based on a semi-quantitative food frequency and demographic lifestyle questionnaire; and venous anti-H. pylori IgG antibodies were tested by ELISA. Unconditional logistic regression analysis with adjustment for potential confounding was performed to estimate the association between target exposures and stomach cancer. RESULTS: An increase in antibody level was related to an elevated odds of stomach cancer (Fifth versus bottom quintile, OR=3.07; 95%CI: 1.16, 8.12; p for trend = 0.032). Compared to participants who were negative with both H. pylori infection and tobacco smoking (either cigarette or waterpipe tobacco), individuals exposed to both these factors showed significantly greater odds of stomach cancer (OR=3.58. (95%CI: 1.32, 9.76, p=0.013). A similar combined impact of H. pylori infection and tobacco smoking was found in individuals who smoked a cigarette (excluded exclusive waterpipe tobacco smokers, ORs = 3.17; 95%CI: 1.13, 8.94, p=0.029) or waterpipe tobacco (excluded exclusive cigarette smokers; OR= 3.96, 95%CI: 1.28, 12.26, p=0.017). CONCLUSIONS: The present study suggests an interaction between H. pylori infection and tobacco smoking, even waterpipe tobacco, to induce stomach cancer.


Assuntos
Infecções por Helicobacter , Helicobacter pylori , Neoplasias Gástricas , Tabaco para Cachimbos de Água , Estudos de Casos e Controles , Infecções por Helicobacter/complicações , Humanos , Masculino , Fumar/efeitos adversos , Neoplasias Gástricas/epidemiologia , Neoplasias Gástricas/etiologia , Fumar Tabaco/efeitos adversos
12.
Nutrients ; 14(7)2022 Mar 24.
Artigo em Inglês | MEDLINE | ID: mdl-35405977

RESUMO

Lung cancer is one of the most common neoplasms globally, with about 2.2 million new cases and 1.8 million deaths annually. Although the most important factor in reducing lung cancer risk is lifestyle change, most patients favour the use of supplements, for example, rather than quitting smoking or following a healthy diet. To better understand the efficacy of such interventions, a systematic review was performed of data from randomized controlled trials concerning the influence of beta-carotene supplementation on lung cancer risk in subjects with no lung cancer before the intervention. The search corpus comprised a number of databases and eight studies involving 167,141 participants, published by November 2021. The findings indicate that beta-carotene supplementation was associated with an increased risk of lung cancer (RR = 1.16, 95% CI = 1.06-1.26). This effect was even more noticeable among smokers and asbestos workers (RR = 1.21, 95% CI = 1.08-1.35) and non-medics (RR = 1.18, 95% CI = 1.07-1.29). A meta-regression found no relationship between the beta-carotene supplementation dose and the size of the negative effect associated with lung cancer risk. Our findings indicate that beta-carotene supplementation has no effect on lung cancer risk. Moreover, when used as the primary chemoprevention, beta-carotene may, in fact, increase the risk of lung cancer.


Assuntos
Neoplasias Pulmonares , beta Caroteno , Antioxidantes/uso terapêutico , Suplementos Nutricionais , Humanos , Neoplasias Pulmonares/tratamento farmacológico , Neoplasias Pulmonares/epidemiologia , Neoplasias Pulmonares/prevenção & controle , Fumar/efeitos adversos , beta Caroteno/uso terapêutico
14.
Nat Genet ; 54(4): 492-498, 2022 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-35410377

RESUMO

Although lung cancer risk among smokers is dependent on smoking dose, it remains unknown if this increased risk reflects an increased rate of somatic mutation accumulation in normal lung cells. Here, we applied single-cell whole-genome sequencing of proximal bronchial basal cells from 33 participants aged between 11 and 86 years with smoking histories varying from never-smoking to 116 pack-years. We found an increase in the frequency of single-nucleotide variants and small insertions and deletions with chronological age in never-smokers, with mutation frequencies significantly elevated among smokers. When plotted against smoking pack-years, mutations followed the linear increase in cancer risk until about 23 pack-years, after which no further increase in mutation frequency was observed, pointing toward individual selection for mutation avoidance. Known lung cancer-defined mutation signatures tracked with both age and smoking. No significant enrichment for somatic mutations in lung cancer driver genes was observed.


Assuntos
Neoplasias Pulmonares , Análise de Célula Única , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Envelhecimento/genética , Criança , Células Epiteliais , Receptores ErbB/genética , Humanos , Neoplasias Pulmonares/genética , Pessoa de Meia-Idade , Mutação , Fumar/efeitos adversos , Fumar/genética , Adulto Jovem
15.
Optom Vis Sci ; 99(4): 358-362, 2022 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-35383735

RESUMO

SIGNIFICANCE: The current study compares the ocular tear film parameters in three different groups using a single noninvasive, practical, and easy-to-use tool. PURPOSE: This study aimed to assess the tear film in smokers, those with a high body mass index (BMI), and healthy subjects using the EASYTEAR view+. METHODS: Thirty men with a high BMI (>25 kg/m2; 24.4 ± 6.4 years), 30 smokers (25.1 ± 6.1 years), and 30 healthy subjects (22.2 ± 3.5 years) were recruited. Each subject completed the Ocular Surface Disease Index, followed by the assessment of noninvasive tear breakup time, tear meniscus height (TMH), and lipid layer patterns (LLPs). RESULTS: Significant differences were found in the median TMH scores between smokers and healthy subjects (P = .03) and between subjects with a high BMI and the healthy ones (P = .04). The median LLP score was significantly (P < .001) higher in normal subjects (4.0 [1.0]) than in smokers (2.4 [1.0]) and subjects with high BMI (2.0 [1.3]). For subjects with a high BMI, the noninvasive tear breakup time score was strongly correlated (Spearman rank correlation coefficient; r) with TMH (r = 0.552, P = .002) and LLP (r = 0.555, P = .001). The LLP showed that grade B (lipid layer thickness, 30 to 50 nm; more compact) was common in subjects with a high BMI, grade C (50 to 80 nm, gray waves) was predominant in smokers, and grade D (~80 nm, dense white-blue layer) represented the majority of normal eye subjects. CONCLUSIONS: Smokers and individuals with a high BMI showed significantly lower lipid layer grades and tear meniscus height scores compared with the control group. The assessment of tear film parameters using the EASYTEAR view+ supports the findings of previous studies that implicate smoking and high BMI as risk factors for dry eye.


Assuntos
Síndromes do Olho Seco , Fumantes , Índice de Massa Corporal , Síndromes do Olho Seco/diagnóstico , Síndromes do Olho Seco/etiologia , Humanos , Masculino , Fumar/efeitos adversos , Lágrimas
16.
Pancreas ; 51(2): 190-195, 2022 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-35404896

RESUMO

OBJECTIVE: Cigarette smoking is an established risk factor for pancreatic ductal adenocarcinoma (PDAC). In this project, we investigated the effect of smoking and the role of histone deacetylase 4 (HDAC4) in PDAC invasion and metastasis. METHODS: Cells were treated with 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and cigarette smoke extract and the mRNA levels of HDACs were measured by real-time polymerase chain reaction. Invasion was measured using the Matrigel Invasion Assay. Syngeneic PDAC mice were treated with 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and metastasis measured. Human PDAC primary and metastatic tissues were analyzed by immunohistochemistry. RESULTS: Levels of HDAC4 mRNA were increased by smoking. Smoking compounds significantly promoted invasion of cancer cells and promoted metastasis of PDAC cells to different organs, including the liver and the lung, whereas inhibition of HDAC4 prevented this effect. The effect of HDAC4 inhibition on preventing smoking-induced metastasis was greater in the liver compared with the lung. We found that HDAC4 is highly expressed in primary and metastatic PDAC tumors. CONCLUSIONS: We found that HDAC4 is the only HDAC induced by smoking among all HDACs analyzed. We found that smoking promotes invasion and metastasis of PDAC cells through a mechanism that involves HDAC4 and that HDAC4 is a promising target for preventing PDAC metastasis.


Assuntos
Carcinoma Ductal Pancreático , Neoplasias Pancreáticas , Animais , Carcinoma Ductal Pancreático/patologia , Linhagem Celular Tumoral , Regulação Neoplásica da Expressão Gênica , Histona Desacetilases/genética , Humanos , Camundongos , Metástase Neoplásica , Neoplasias Pancreáticas/genética , Neoplasias Pancreáticas/patologia , RNA Mensageiro , Proteínas Repressoras/genética , Fumar/efeitos adversos
17.
Sci Rep ; 12(1): 6231, 2022 Apr 14.
Artigo em Inglês | MEDLINE | ID: mdl-35422064

RESUMO

Tobacco use is the leading preventable cause of cancer, and affects the respiratory, oral, fecal, and duodenal mucosa-associated microbiota. However, the effects of smoking on the duodenal luminal microbiome have not been studied directly. We aimed to compare the duodenal luminal microbiome in never-smokers, current smokers, and ex-smokers who quit ≥ 10 years ago. In a cross-sectional study, current smokers (CS, n = 24) were identified and matched to never-smokers (NS, n = 27) and ex-smokers (XS, n = 27) by age (± 5 years), body mass index (BMI, ± 3 kg/m2), and sex. Current antibiotic users were excluded. The duodenal luminal microbiome was analysed in 1 aspirate sample per subject by 16S rRNA gene sequencing. Relative abundances (RA) of families associated with increased duodenal microbial diversity, Prevotellaceae, Neisseriaceae, and Porphyromonadaceae, were significantly lower in CS vs. NS. This was driven by lower RA of unknown Prevotella and Porphyromonas species, and Neisseria subflava and N. cinerea, in CS. In contrast, RA of Enterobacteriaceae and Lactobacillaceae (associated with decreased diversity), were significantly higher in CS, due to higher RA of Escherichia-Shigella, Klebsiella and Lactobacillus species. Many of these changes were absent or less pronounced in XS, who exhibited a duodenal luminal microbiome more similar to NS. RA of taxa previously found to be increased in the oral and respiratory microbiota of smokers were also higher in the duodenal luminal microbiome, including Bulledia extructa and an unknown Filifactor species. In conclusion, smoking is associated with an altered duodenal luminal microbiome. However, ex-smokers have a duodenal luminal microbiome that is similar to never-smokers.


Assuntos
Microbiota , Fumar , Estudos Transversais , Humanos , RNA Ribossômico 16S/genética , Fumar/efeitos adversos , Fumar Tabaco
18.
Atherosclerosis ; 348: 36-43, 2022 05.
Artigo em Inglês | MEDLINE | ID: mdl-35405480

RESUMO

BACKGROUND AND AIMS: Studies of self-reported coffee consumption and smoking on risk of dementia have shown results conflicting with two-sample Mendelian randomization studies. We tested the hypotheses that coffee consumption and smoking influence risk of dementia using observational and one-sample Mendelian randomization designs with individual level data. METHODS: We included 114,551 individuals from two Danish general population cohorts (median age 58 years). First, we tested whether high self-reported coffee consumption/smoking were associated with risk of dementia. Second, whether genetically predicted high coffee consumption/smoking due to variation near CYP1A1/AHR/CHRNA3 genes were associated with risk of dementia. RESULTS: We observed 3,784 dementia events. Moderate self-reported coffee consumption was associated with low risk of all dementia and non-Alzheimer's dementia, with a similar trend for Alzheimer's disease. Genetically predicted high coffee consumption was associated with high risk of all dementia (hazard ratio [95% confidence interval] per +1 cup/day: 1.20 [1.01-1.42]), with a similar trend for non-Alzheimer's dementia (1.23 [0.95-1.53]). High self-reported smoking was associated with high risk of non-Alzheimer's dementia. High genetically predicted smoking was associated with a trend towards high risk of all dementia and Alzheimer's disease (hazard ratios per +1 pack-year: 1.04 [0.96-1.11]) and 1.06 [0.97-1.16]). CONCLUSIONS: Moderate self-reported coffee consumption was associated with low risk of all and non-Alzheimer's dementia, while high genetically predicted coffee consumption was associated with a trend towards the opposite. High self-reported smoking was associated with high risk of non-Alzheimer's dementia, with a similar trend for genetically predicted smoking on all dementia and Alzheimer's disease.


Assuntos
Doença de Alzheimer , Café , Humanos , Análise da Randomização Mendeliana , Pessoa de Meia-Idade , Fatores de Risco , Autorrelato , Fumar/efeitos adversos , Fumar/genética
19.
J Periodontal Res ; 57(3): 587-593, 2022 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-35415888

RESUMO

BACKGROUND AND OBJECTIVES: Several epidemiological studies have reported that smokers have a higher prevalence and severity of periodontal disease than do nonsmokers, and that smoking negatively affects nutritional status and is associated with a reduced intake of antioxidants, particularly vitamin C. The present investigation aimed to examine the relationship between serum vitamin C levels and smoking and its influence on the periodontal condition in older adults. MATERIALS AND METHODS: A total of 353 respondents met the inclusion criteria and were enrolled in the present study. The periodontal status of the study participants was determined through examinations of one or more residual teeth, which included a measurement of the probing pocket depth (PPD) and clinical attachment level (CAL) at six regions of each tooth. Blood samples were collected during the dental examinations and then sent to a laboratory to evaluate serum vitamin C and cotinine levels. A serum cotinine concentration of 100 ng/ml was considered a relevant threshold for active smoking. After dividing the participants into two groups according to serum cotinine levels, Poisson regression analysis was carried out to compare vitamin C levels with the prevalence rate ratio (PRR) for periodontal condition markers for each group based on serum cotinine levels. RESULTS: We evaluated differences in the PRR of serum vitamin C tertiles between participants with high (≥100 ng/ml) or low (<100 ng/ml) serum cotinine levels after adjusting for sex, the use of interdental brushes or dental floss, and the number of teeth. A negative tendency between the PRR of vitamin C tertiles for the PPD or CAL was seen for both groups. Especially, a bigger difference was observed in the group with high serum cotinine levels. The PRR of the first tertiles in the high serum cotinine group was 5.03, compared with 2.69 in the low serum cotinine group (relative risk: 1.9). CONCLUSION: The results of this study suggest a potential association between vitamin C levels and the periodontal condition, which may be influenced by smoking status.


Assuntos
Cotinina , Doenças Periodontais , Idoso , Ácido Ascórbico , Cotinina/análise , Humanos , Fumar/efeitos adversos , Tuberculina
20.
Pancreatology ; 22(4): 507-515, 2022 May.
Artigo em Inglês | MEDLINE | ID: mdl-35422382

RESUMO

BACKGROUND: Early-onset pancreatic cancer (≤50 years, EOPC) is uncommon. This study aims to characterize the clinical and survival characteristics of EOPC in comparison to late-onset pancreatic cancer (>50 years, LOPC). METHODS: We retrospectively investigated consecutive PC patients treated at our institution between 2010 and 2019. We analyzed and compared clinicopathological characteristics, treatments, and outcomes of EOPC and LOPC. RESULTS: Of 1646 PC patients identified (768 resectable/borderline resectable; 248 locally advanced; 630 metastatic), 127 (8%) had EOPC. Current smoking and heavy drinking were associated with EOPC. EOPC presented at a more advanced stage and had higher neutrophil-to-lymphocyte ratios than LOPC. Survival outcomes were similar between the two groups, both in the entire cohort and in each resectability group. In patients undergoing resection, EOPC tended to have a higher N stage (p = 0.099) and had a higher pathological stage (stage IV, 20% vs. 7%, p = 0.005) and a lower rate of macroscopically curative resection (80% vs. 93%, p = 0.006). Liver recurrence was more commonly observed in EOPC (42% vs. 23%, p = 0.015). In the metastatic cohort, combination chemotherapy regimens were more frequently administered in EOPC as first-line treatment (79% vs. 64%, p = 0.028). Both median PFS (4.4 vs. 5.3 months, p = 0.647) and OS (11.5 vs. 9.5 months, p = 0.183) were not significantly different between the two groups. CONCLUSIONS: EOPC presented with a more aggressive tumor biology. Survival outcomes were similar to LOPC due to more intensive treatment.


Assuntos
Neoplasias Pancreáticas , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Estudos de Coortes , Humanos , Terapia Neoadjuvante , Neoplasias Pancreáticas/cirurgia , Estudos Retrospectivos , Fumar/efeitos adversos
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA