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1.
PLoS One ; 19(6): e0304473, 2024.
Artículo en Inglés | MEDLINE | ID: mdl-38848350

RESUMEN

PURPOSE: We performed a meta-analysis to identify risk factors affecting spinal fusion. METHODS: We systematically searched PubMed, Embase, and the Cochrane Library from inception to January 6, 2023, for articles that report risk factors affecting spinal fusion. The pooled odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using fixed-effects models for each factor for which the interstudy heterogeneity I2 was < 50%, while random-effects models were used when the interstudy heterogeneity I2 was ≥ 50%. Using sample size, Egger's P value, and heterogeneity across studies as criteria, we categorized the quality of evidence from observational studies as high-quality (Class I), moderate-quality (Class II or III), or low-quality (Class IV). Furthermore, the trim-and-fill procedure and leave-one-out protocol were conducted to investigate potential sources of heterogeneity and verify result stability. RESULTS: Of the 1,257 citations screened, 39 unique cohort studies comprising 7,145 patients were included in the data synthesis. High-quality (Class I) evidence showed that patients with a smoking habit (OR, 1.57; 95% CI, 1.11 to 2.21) and without the use of bone morphogenetic protein-2 (BMP-2) (OR, 4.42; 95% CI, 3.33 to 5.86) were at higher risk for fusion failure. Moderate-quality (Class II or III) evidence showed that fusion failure was significantly associated with vitamin D deficiency (OR, 2.46; 95% CI, 1.24 to 4.90), diabetes (OR, 3.42; 95% CI, 1.59 to 7.36), allograft (OR, 1.82; 95% CI, 1.11 to 2.96), conventional pedicle screw (CPS) fixation (OR, 4.77; 95% CI, 2.23 to 10.20) and posterolateral fusion (OR, 3.63; 95% CI, 1.25 to 10.49). CONCLUSIONS: Conspicuous risk factors affecting spinal fusion include three patient-related risk factors (smoking, vitamin D deficiency, and diabetes) and four surgery-related risk factors (without the use of BMP-2, allograft, CPS fixation, and posterolateral fusion). These findings may help clinicians strengthen awareness for early intervention in patients at high risk of developing fusion failure.


Asunto(s)
Fusión Vertebral , Fusión Vertebral/efectos adversos , Humanos , Factores de Riesgo , Estudios de Cohortes , Proteína Morfogenética Ósea 2 , Fumar/efectos adversos
3.
Nat Commun ; 15(1): 4909, 2024 Jun 08.
Artículo en Inglés | MEDLINE | ID: mdl-38851766

RESUMEN

Tobacco smoking (TS) is implicated in lung cancer (LC) progression through the development of metabolic syndrome. However, direct evidence linking metabolic syndrome to TS-mediated LC progression remains to be established. Our findings demonstrate that 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and benzo[a]pyrene (NNK and BaP; NB), components of tobacco smoke, induce metabolic syndrome characteristics, particularly hyperglycemia, promoting lung cancer progression in male C57BL/6 J mice. NB enhances glucose uptake in tumor-associated macrophages by increasing the expression and surface localization of glucose transporter (GLUT) 1 and 3, thereby leading to transcriptional upregulation of insulin-like growth factor 2 (IGF2), which subsequently activates insulin receptor (IR) in LC cells in a paracrine manner, promoting its nuclear import. Nuclear IR binds to nucleophosmin (NPM1), resulting in IR/NPM1-mediated activation of the CD274 promoter and expression of programmed death ligand-1 (PD-L1). Restricting glycolysis, depleting macrophages, or blocking PD-L1 inhibits NB-mediated LC progression. Analysis of patient tissues and public databases reveals elevated levels of IGF2 and GLUT1 in tumor-associated macrophages, as well as tumoral PD-L1 and phosphorylated insulin-like growth factor 1 receptor/insulin receptor (pIGF-1R/IR) expression, suggesting potential poor prognostic biomarkers for LC patients. Our data indicate that paracrine IGF2/IR/NPM1/PD-L1 signaling, facilitated by NB-induced dysregulation of glucose levels and metabolic reprogramming of macrophages, contributes to TS-mediated LC progression.


Asunto(s)
Antígeno B7-H1 , Benzo(a)pireno , Progresión de la Enfermedad , Hiperglucemia , Factor II del Crecimiento Similar a la Insulina , Neoplasias Pulmonares , Ratones Endogámicos C57BL , Proteínas Nucleares , Nucleofosmina , Receptor de Insulina , Animales , Neoplasias Pulmonares/metabolismo , Neoplasias Pulmonares/patología , Neoplasias Pulmonares/genética , Masculino , Humanos , Receptor de Insulina/metabolismo , Receptor de Insulina/genética , Ratones , Antígeno B7-H1/metabolismo , Antígeno B7-H1/genética , Hiperglucemia/metabolismo , Benzo(a)pireno/toxicidad , Factor II del Crecimiento Similar a la Insulina/metabolismo , Factor II del Crecimiento Similar a la Insulina/genética , Proteínas Nucleares/metabolismo , Proteínas Nucleares/genética , Nitrosaminas/toxicidad , Macrófagos Asociados a Tumores/metabolismo , Línea Celular Tumoral , Comunicación Paracrina , Regulación Neoplásica de la Expresión Génica , Fumar/efectos adversos , Macrófagos/metabolismo
4.
Int J Chron Obstruct Pulmon Dis ; 19: 1233-1245, 2024.
Artículo en Inglés | MEDLINE | ID: mdl-38854590

RESUMEN

Purpose: Smoking is a major risk factor for the group 3 PH. NT-proBNP is a biomarker for risk stratification in PH. This study aims to investigate the effects of smoking status and smoking index (SI) on group 3 PH and to evaluate the value of SI and SI combined with NT-proBNP in early diagnosis and prediction of disease severity. Patients and Methods: Four hundred patients with group 3 PH at the First Hospital of Shanxi Medical University between January 2020 and December 2021 were enrolled and divided into two groups: mild (30 mmHg ≤ pulmonary artery systolic pressure (PASP)≤50 mmHg) and non-mild (PASP >50 mmHg). The effect of smoking on group 3 PH was analyzed using univariate analysis, and logistic analysis was conducted to evaluate the risk of group 3 PH according to smoking status and SI. Spearman correlation coefficient was used to test the correlation between SI and the index of group 3 PH severity. The predictive value of SI was evaluated using a receiver operating characteristic (ROC) curve. Results: Correlation and logistic analyses showed that SI was associated with PH severity. Smoking status (P=0.009) and SI (P=0.039) were independent risk factors for non-mild group 3 PH, and ROC showed that the predictive value of SI (AUC:0.596) for non-mild PH was better than that of the recognized pro-brain natriuretic peptide (NT-proBNP) (AUC:0.586). SI can be used as a single predictive marker. SI and NT-proBNP can be formulated as prediction models for screening non-mild clinical cases (AUC:0.628). Conclusion: SI is a potentially ideal non-invasive predictive marker for group 3 PH. SI and NT-proBNP could be used to develop a prediction model for screening non-mild PH cases. This can greatly improve the predictive specificity of the established PH marker, NT-proBNP.


Asunto(s)
Biomarcadores , Hipertensión Pulmonar , Péptido Natriurético Encefálico , Fragmentos de Péptidos , Valor Predictivo de las Pruebas , Índice de Severidad de la Enfermedad , Fumar , Humanos , Péptido Natriurético Encefálico/sangre , Fragmentos de Péptidos/sangre , Femenino , Masculino , Persona de Mediana Edad , Estudios Retrospectivos , Biomarcadores/sangre , Fumar/efectos adversos , Fumar/sangre , Fumar/epidemiología , Hipertensión Pulmonar/sangre , Hipertensión Pulmonar/diagnóstico , Hipertensión Pulmonar/fisiopatología , Hipertensión Pulmonar/etiología , Anciano , Factores de Riesgo , Medición de Riesgo , Pronóstico , Enfermedad Pulmonar Obstructiva Crónica/sangre , Enfermedad Pulmonar Obstructiva Crónica/diagnóstico , Enfermedad Pulmonar Obstructiva Crónica/fisiopatología , Enfermedad Pulmonar Obstructiva Crónica/complicaciones , China/epidemiología , Adulto , Presión Arterial
5.
Sci Rep ; 14(1): 13825, 2024 06 15.
Artículo en Inglés | MEDLINE | ID: mdl-38879601

RESUMEN

The purpose of this study was to investigate the causal association between unhealthy lifestyle style factors and the risk of colorectal cancer, with the aim of preventing the occurrence of colorectal cancer by modifying unhealthy lifestyles. A two-sample Mendelian randomization (MR) approach was employed in this study, utilizing the inverse-variance weighted method as the primary research method. This MR analysis analyzed data of 3022 colorectal cancer cases and 174,006 controls from the FinnGen database. Single nucleotide polymorphisms (SNPs) associated with unhealthy lifestyle factors were selected as instrumental variables (IVs), including two obesity-related indicators, BMI (body mass index) and WHR (waist-to-hip ratio). Four phenotypes of smoking (smoking initiation, ever smoked, smoking per day, smoking cessation) and one phenotype of alcohol consumption (drinks per week). Four phenotypes of physical activity (accelerometer-based physical activity, moderate-to-vigorous physical activity, vigorous physical activity, strenuous sports or other exercises). All SNPs were obtained from published genome-wide association studies. The study found that the obesity-related indicator, higher WHR (OR = 1.38, 95% CI 1.12-1.70; P = 0.002) were associated with an increased risk of colorectal cancer, and two smoking phenotypes, cigarettes per day(OR = 1.30, 95% CI 1.01-1.68; P = 0.042)and smoking initiation (OR = 3.48, 95% CI 1.15-10.55; P = 0.028), were potentially associated with an increased risk of colorectal cancer. However, there was no evidence to suggest that physical activities and alcohol consumption were associated with colorectal cancer (all p > 0.05). In addition, the study detected no pleiotropy (all p > 0.05). This MR analysis indicates a causal association between a higher waist-to-hip ratio and the risk of colorectal cancer and a suggestive association between smoking and the risk of colorectal cancer among Europeans. These findings contribute to the understanding of the etiology of colorectal cancer and have potential implications for its prevention.


Asunto(s)
Neoplasias Colorrectales , Estilo de Vida , Análisis de la Aleatorización Mendeliana , Polimorfismo de Nucleótido Simple , Fumar , Humanos , Neoplasias Colorrectales/genética , Neoplasias Colorrectales/epidemiología , Neoplasias Colorrectales/etiología , Factores de Riesgo , Fumar/efectos adversos , Ejercicio Físico , Estudio de Asociación del Genoma Completo , Consumo de Bebidas Alcohólicas/efectos adversos , Consumo de Bebidas Alcohólicas/genética , Masculino , Índice de Masa Corporal , Femenino , Obesidad/genética , Obesidad/epidemiología , Relación Cintura-Cadera
6.
Respir Res ; 25(1): 240, 2024 Jun 12.
Artículo en Inglés | MEDLINE | ID: mdl-38867225

RESUMEN

BACKGROUND: Despite the success of antiretroviral therapy (ART), people living with HIV (PLWH) suffer from a high burden of pulmonary diseases, even after accounting for their smoking status. Cytotoxic CD8 T-cells are likely implicated in this phenomenon and may act as a double-edged sword. While being essential in viral infection control, their hyperactivation can also contribute to lung mucosal tissue damage. The effects of HIV and smoking on pulmonary mucosal CD8 T-cell dynamics has been a neglected area of research, which we address herein. METHODS: Bronchoalveolar lavage (BAL) fluid were obtained from ART-treated PLWH (median duration of supressed viral load: 9 years; smokers: n = 14; non-smokers: n = 21) and HIV-uninfected controls (smokers: n = 11; non-smokers: n = 20) without any respiratory symptoms or active infection. Lymphocytes were isolated and CD8 T-cell subsets and homing markers were characterized by multiparametric flow cytometry. RESULTS: Both smoking and HIV infection were independently associated with a significant increase in frequencies of total pulmonary mucosal CD8 T-cell. BAL CD8 T-cells were primarily CD69 + expressing CD103 and/or CD49a, at least one of the two granzymes (GzmA/GzmB), and little Perforin. Higher expression levels of CD103, CD69, and GzmB were observed in smokers versus non-smokers. The ex vivo phenotype of GzmA + and GzmB + cells revealed increased expression of CD103 and CXCR6 in smokers, while PLWH displayed elevated levels of CX3CR1 compared to controls. CONCLUSION: Smoking and HIV could promote cytotoxic CD8 T-cell retention in small airways through different mechanisms. Smoking likely increases recruitment and retention of GzmB + CD8 Trm via CXCR6 and CD103. Heightened CX3CR1 expression could be associated with CD8 non-Trm recruitment from the periphery in PLWH.


Asunto(s)
Infecciones por VIH , Humanos , Masculino , Infecciones por VIH/tratamiento farmacológico , Infecciones por VIH/inmunología , Femenino , Persona de Mediana Edad , Adulto , Mucosa Respiratoria/inmunología , Mucosa Respiratoria/metabolismo , Mucosa Respiratoria/efectos de los fármacos , Linfocitos T CD8-positivos/inmunología , Linfocitos T CD8-positivos/efectos de los fármacos , Linfocitos T CD8-positivos/metabolismo , Linfocitos T Citotóxicos/inmunología , Linfocitos T Citotóxicos/efectos de los fármacos , Linfocitos T Citotóxicos/metabolismo , Fumar/efectos adversos , Líquido del Lavado Bronquioalveolar/inmunología , Antirretrovirales/uso terapéutico , Fármacos Anti-VIH/uso terapéutico , Pulmón/inmunología , Pulmón/efectos de los fármacos , Pulmón/metabolismo
7.
Respir Med ; 230: 107684, 2024.
Artículo en Inglés | MEDLINE | ID: mdl-38823564

RESUMEN

BACKGROUND: An increased incidence of pneumomediastinum has been observed among patients hospitalized with coronavirus disease 2019 (COVID-19) pneumonia. The study aimed to identify risk factors for COVID-19-associated pneumomediastinum and investigate the impact of pneumomediastinum on clinical outcomes. METHODS: In this multicentre retrospective case-control study, we included consecutive patients with COVID-19 pneumonia and pneumomediastinum hospitalized from March 2020 to July 2020 at ten centres; then, we identified a similarly sized control group of consecutive patients hospitalized with COVID-19 pneumonia and respiratory failure who did not develop pneumomediastinum during the same period. Clinical, laboratory, and radiological characteristics, as well as respiratory support and outcomes, were collected and compared between the two groups. Risk factors of pneumomediastinum were assessed by multivariable logistic analysis. RESULTS: Overall 139 patients with pneumomediastinum and 153 without pneumomediastinum were analysed. Lung involvement ≥75 %, consolidations, body mass index (BMI) < 22 kg/m2, C-reactive protein (CRP) > 150 mg/L, D-dimer >3000 ng/mL FEUs, and smoking exposure >20 pack-year were all independently correlated with the occurrence of pneumomediastinum. Patients with pneumomediastinum had a longer hospital stay (mean ± SD 31.2 ± 20.2 days vs 19.6 ± 14.2, p < 0.001), higher intubation rate (73/139, 52.5 % vs 27/153, 17.6 %, p < 0.001), and in-hospital mortality (68/139, 48.9 % vs 36/153, 23.5 %, p < 0.001) compared to controls. CONCLUSIONS: Extensive lung parenchyma involvement, consolidations, low BMI, high inflammatory markers, and tobacco exposure are associated with a greater risk of pneumomediastinum in COVID-19 pneumonia. This complication significantly worsens the outcomes.


Asunto(s)
COVID-19 , Enfisema Mediastínico , Humanos , Enfisema Mediastínico/etiología , Enfisema Mediastínico/diagnóstico por imagen , COVID-19/complicaciones , Masculino , Factores de Riesgo , Femenino , Estudios de Casos y Controles , Persona de Mediana Edad , Estudios Retrospectivos , Anciano , Proteína C-Reactiva/metabolismo , Proteína C-Reactiva/análisis , Tiempo de Internación , SARS-CoV-2 , Índice de Masa Corporal , Fumar/efectos adversos , Fumar/epidemiología , Hospitalización/estadística & datos numéricos , Adulto
8.
Ren Fail ; 46(1): 2356024, 2024 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-38832473

RESUMEN

OBJECTIVE: Smoking has been suggested as a modifiable and cardiovascular risk factor for chronic kidney disease (CKD). Although long-term smoking has been associated with CKD, the potential relationship between its metabolite hydroxycotinine and CKD has not been clarified. METHODS: A total of 8,544 participants aged 20 years and above from the National Health and Nutrition Examination Survey (NHANES) 2017 - March 2020 were enrolled in our study. CKD was defined by estimated glomerular filtration rate (eGFR) < 60 mL/(min*1.73 m2). Serum hydroxycotinine was measured by an isotope-dilution high-performance liquid chromatography/atmospheric pressure chemical ionization tandem mass spectrometric (ID HPLC-APCI MS/MS) method with a lower limit of detections (LLOD) at 0.015 ng/mL. The non-linear relationship was explored with restricted cubic splines (RCS). Pearson's correlation coefficient and a multivariate logistic regression model were used for correlation analysis. RESULTS: Serum hydroxycotinine and eGFR were negatively correlated in both non-CKD group (r= -0.05, p < 0.001) and CKD group (r= -0.04, p < 0.001). After serum hydoxycotinine dichotominzed with LLOD, serum hydroxycotinine ≥ 0.015 ng/mL was negatively correlated with eGFR not only in non-CKD group (r = -0.05, p < 0.001) but also in CKD group (r = -0.09, p < 0.001). After adjusting for comprehensive confounders, results from the multivariate logistic regression analysis showed that participants with serum hydroxycotinine ≥ 0.015 ng/mL had increased odds of CKD (OR = 1.505, p < 0.001). CONCLUSIONS: Serum hydroxycotinine might be positively associated with CKD. Further study is warranted to find the right concentration of hydroxycotinine to measure the CKD.


Asunto(s)
Tasa de Filtración Glomerular , Encuestas Nutricionales , Insuficiencia Renal Crónica , Humanos , Masculino , Insuficiencia Renal Crónica/sangre , Femenino , Estudios Transversales , Persona de Mediana Edad , Adulto , Anciano , Espectrometría de Masas en Tándem , Factores de Riesgo , Modelos Logísticos , Cromatografía Líquida de Alta Presión , Fumar/epidemiología , Fumar/efectos adversos , Biomarcadores/sangre , Cotinina/análogos & derivados
9.
BMC Cardiovasc Disord ; 24(1): 292, 2024 Jun 05.
Artículo en Inglés | MEDLINE | ID: mdl-38840064

RESUMEN

BACKGROUND: Tobacco use is recognized as a major cause of cardiovascular disease, which is associated with endothelial dysfunction. Endothelial function is evaluated using flow-mediated dilation (FMD), which is a noninvasive method. This meta-analysis aimed to investigate the association between smoking exposure and endothelial function evaluated using FMD values. METHODS: We searched the PubMed, Embase, Web of Science, and Cochrane Library databases for cohort studies of smokers or passive smokers that used FMD to assess endothelial function. The primary outcome of the study was the change in the rate of FMD. The risk of bias was evaluated using the Cochrane Collaboration tool and Newcastle-Ottawa Scale. Further, the weighted mean difference was used to analyze the continuous data. RESULTS: Overall, 14 of 1426 articles were included in this study. The results of these articles indicated that smoking is a major cause of endothelial dysfunction and altered FMD; a pooled effect size of - 3.15 was obtained with a 95% confidence interval of (- 3.84, - 2.46). Notably, pregnancy status, Asian ethnicity, or health status did not affect heterogeneity. CONCLUSIONS: We found that smoking has a significant negative impact on FMD, and measures such as medication or education for smoking cessation may improve endothelial function and reduce the risk of cardiovascular disease. TRIAL REGISTRATION: The meta-analysis was registered with PROSPERO on April 5th, 2023 (CRD42023414654).


Asunto(s)
Enfermedades Cardiovasculares , Endotelio Vascular , Vasodilatación , Humanos , Endotelio Vascular/fisiopatología , Femenino , Masculino , Persona de Mediana Edad , Adulto , Medición de Riesgo , Enfermedades Cardiovasculares/fisiopatología , Enfermedades Cardiovasculares/diagnóstico , Enfermedades Cardiovasculares/etiología , Enfermedades Cardiovasculares/epidemiología , Anciano , Factores de Riesgo , Contaminación por Humo de Tabaco/efectos adversos , Valor Predictivo de las Pruebas , Fumar/efectos adversos , Fumar/fisiopatología , Adulto Joven , Fumadores , Arteria Braquial/fisiopatología , Arteria Braquial/diagnóstico por imagen , Factores de Riesgo de Enfermedad Cardiaca
10.
Rev Prat ; 74(5): 526-528, 2024 May.
Artículo en Francés | MEDLINE | ID: mdl-38833236

RESUMEN

SMOKING AND TUBERCULOSIS. Tuberculosis and smoking are responsible for high mortality worldwide. Tuberculosis causes 9 million incident cases and 1.6 million deaths every year. Smoking increases the risk of infection by Mycobacterium tuberculosis and of severe tuberculosis disease with death or recurrence. Cessation of smoking improves the course of the disease, promoting adherence to anti-tuberculosis treatment and definitive cure. All health-care professionals involved in tuberculosis care must be involved to help smokers with tuberculosis to quit.


TABAC ET TUBERCULOSE. La tuberculose et le tabagisme sont à l'origine d'une importante mortalité dans le monde. La tuberculose cause 9 millions de cas incidents et 1,6 million de décès chaque année. Le tabagisme augmente les risques d'infection par Mycobacterium tuberculosis et de tuberculose maladie sévère avec décès ou récidive. L'arrêt du tabac améliore le cours de l'infection, favorisant l'adhésion des patients au traitement antituberculeux et la guérison définitive. Tous les professionnels de santé doivent s'investir dans la mission d'aide à l'arrêt du tabac des fumeurs atteints de tuberculose.


Asunto(s)
Cese del Hábito de Fumar , Fumar , Tuberculosis , Humanos , Tuberculosis/epidemiología , Tuberculosis/prevención & control , Fumar/efectos adversos , Fumar/epidemiología , Cese del Hábito de Fumar/métodos , Factores de Riesgo
11.
BMC Musculoskelet Disord ; 25(1): 433, 2024 Jun 03.
Artículo en Inglés | MEDLINE | ID: mdl-38831392

RESUMEN

This study presents a systematic literature review and meta-analysis of pseudarthrosis risk factors following lumbar fusion procedures. The odds ratio (OR) and 95% confidence interval (95% CI) were used for outcome measurements. The objective of this study was to identify the independent risk factors for pseudarthrosis after lumbar spinal fusion, which is crucial for mitigating morbidity and reoperation. Systematic searches in PubMed, Embase, and Scopus (1990-July 2021) were conducted using specific terms. The inclusion criteria included prospective and retrospective cohorts and case‒control series reporting ORs with 95% CIs from multivariate analysis. The quality assessment utilized the Newcastle-Ottawa scale. Meta-analysis, employing OR and 95% CI, assessed pseudarthrosis risk factors in lumbar fusion surgery, depicted in a forest plot. Of the 568 abstracts identified, 12 met the inclusion criteria (9 retrospective, 2006-2021). The 17 risk factors were categorized into clinical, radiographic, surgical, and bone turnover marker factors. The meta-analysis highlighted two significant clinical risk factors: age (95% CI 1.02-1.11; p = 0.005) and smoking (95% CI 1.68-5.44; p = 0.0002). The sole significant surgical risk factor was the number of fused levels (pooled OR 1.35; 95% CI 1.17-1.55; p < 0.0001). This study identified 17 risk factors for pseudarthrosis after lumbar fusion surgery, emphasizing age, smoking status, and the number of fusion levels. Prospective studies are warranted to explore additional risk factors and assess the impact of surgery and graft type.


Asunto(s)
Vértebras Lumbares , Seudoartrosis , Fusión Vertebral , Humanos , Fusión Vertebral/efectos adversos , Seudoartrosis/etiología , Seudoartrosis/epidemiología , Vértebras Lumbares/cirugía , Vértebras Lumbares/diagnóstico por imagen , Factores de Riesgo , Factores de Edad , Fumar/efectos adversos
12.
Am J Case Rep ; 25: e943909, 2024 Jun 18.
Artículo en Inglés | MEDLINE | ID: mdl-38889103

RESUMEN

BACKGROUND A 52-year-old male patient presented with symptoms of chronic cough and persistent tracheal irritation 26 years after surgical closure of a tracheostoma, supported by an autologous auricular cartilage graft and cutaneous transplant. At the initial clinical presentation, the patient was an active smoker, with a cumulative dose of 31 pack years. CASE REPORT Bronchoscopy revealed endotracheal hair growth and local inflammation at the graft site. Initial anti-inflammatory, antimycotic, and antibacterial therapy was administered, followed by endoscopic structure remodeling. There were multiple recurrences with similar symptoms, showing isolated hair growth, without inflammation. Annual endoscopic restructuring sessions were indicated, and the patient experienced them as highly relieving. Recurrent hair growth was finally terminated by argon plasma laser-coagulation and after smoking cessation. We hypothesize that the onset of hair growth was triggered by the patient's cigarette smoking. CONCLUSIONS Endotracheal hair growth is a potential complication of autograft-supported tracheal restructuring. The initial administration of antimicrobial and anti-inflammatory medication, combined with endoscopic restructuring, could have contained the active inflammation; the application of argon plasma laser-coagulation finally stopped the hair growth. Smoking is associated with the upregulation of molecular signaling pathways in the respiratory epithelium, which can stimulate hair follicles, such as sonic hedgehog protein, WNT-1/ß-catenin, and epidermal growth factor receptor.


Asunto(s)
Cabello , Humanos , Masculino , Persona de Mediana Edad , Broncoscopía , Traqueostomía , Tráquea , Fumar/efectos adversos , Cartílago Auricular , Coagulación con Plasma de Argón , Enfermedades de la Tráquea/etiología
13.
Int J Chron Obstruct Pulmon Dis ; 19: 1315-1331, 2024.
Artículo en Inglés | MEDLINE | ID: mdl-38895046

RESUMEN

Purpose: Cigarette smoking is the most recognized risk factor of chronic obstructive pulmonary disease (COPD) in China. However, there are no studies analyzing the impact of different smoking behaviors on pulmonary function and pulmonary hypertension (PH) among Chinese male patients with COPD. Patients and Methods: Chinese male smokers with COPD performed pulmonary function tests. Clinical characteristics, smoking behavior features, spirometry and echocardiographic results were compared between the two groups stratified by initial smoking age (18 years old) or complicated PH. Results: The early-smoking group had more respiratory symptoms, more severe smoking behavior, worse pulmonary function with lower FEV1%pre (38.5% vs 70.2%) and FEV1/FVC% (47.5% vs 63.8%), and higher systolic pulmonary artery pressure (sPAP: 38.6 vs 33.9 mmHg) than the late-smoking group. Initiating smoking before adulthood was an independently contributing factor of ventilatory dysfunction and Global Initiative for Obstructive Lung Disease (GOLD) stage escalation. It also had a significant interaction with long smoking duration (≥30 years), characterized by markedly decreased lung volumes (VC%pre: 64.0% vs 84.5%), impaired diffusing capacity (DLCO%pre: 58.0% vs 76.8%) and severe emphysema (RV/TLC%pre: 145.2% vs 130.2%). COPD patients complicated with PH exhibited worse ventilatory function (FEV1%pre: 43.2% vs 56.2%), impaired diffusion capacity (DLCO%pre: 56.7% vs 77.1%) and decreased lung volume (VC%pre: 67.67% vs 75.38%). Both severe smoking behaviors and impaired pulmonary function had close correlations with sPAP. Conclusion: The early-smoking group exhibited predominantly ventilation dysfunction and had complex interactions with long smoking duration to further affect lung volume and diffusion capacity. Different smoking behaviors influenced variations of pulmonary dysfunction and comorbid PH in patients with COPD.


Asunto(s)
Hipertensión Pulmonar , Pulmón , Enfermedad Pulmonar Obstructiva Crónica , Fumar , Humanos , Masculino , Enfermedad Pulmonar Obstructiva Crónica/fisiopatología , Enfermedad Pulmonar Obstructiva Crónica/diagnóstico , Enfermedad Pulmonar Obstructiva Crónica/epidemiología , Persona de Mediana Edad , Pulmón/fisiopatología , China/epidemiología , Hipertensión Pulmonar/fisiopatología , Hipertensión Pulmonar/epidemiología , Hipertensión Pulmonar/diagnóstico , Hipertensión Pulmonar/etiología , Factores de Riesgo , Anciano , Volumen Espiratorio Forzado , Fumar/efectos adversos , Fumar/epidemiología , Capacidad Vital , Espirometría , Capacidad de Difusión Pulmonar , Factores de Tiempo , Índice de Severidad de la Enfermedad , Fumadores , Presión Arterial , Arteria Pulmonar/fisiopatología , Estudios Transversales , Pueblos del Este de Asia
14.
RMD Open ; 10(2)2024 Jun 17.
Artículo en Inglés | MEDLINE | ID: mdl-38886003

RESUMEN

OBJECTIVE: To compare longitudinal changes in spirometric measures between patients with rheumatoid arthritis (RA) and non-RA comparators. METHODS: We analysed longitudinal data from two prospective cohorts: the UK Biobank and COPDGene. Spirometry was conducted at baseline and a second visit after 5-7 years. RA was identified based on self-report and disease-modifying antirheumatic drug use; non-RA comparators reported neither. The primary outcomes were annual changes in the per cent-predicted forced expiratory volume in 1 s (FEV1%) and per cent predicted forced vital capacity (FVC%). Statistical comparisons were performed using multivariable linear regression. The analysis was stratified based on baseline smoking status and the presence of obstructive pattern (FEV1/FVC <0.7). RESULTS: Among participants who underwent baseline and follow-up spirometry, we identified 233 patients with RA and 37 735 non-RA comparators. Among never-smoking participants without an obstructive pattern, RA was significantly associated with more FEV1% decline (ß=-0.49, p=0.04). However, in ever smokers with ≥10 pack-years, those with RA exhibited significantly less FEV1% decline than non-RA comparators (ß=0.50, p=0.02). This difference was more pronounced among those with an obstructive pattern at baseline (ß=1.12, p=0.01). Results were similar for FEV1/FVC decline. No difference was observed in the annual FVC% change in RA versus non-RA. CONCLUSIONS: Smokers with RA, especially those with baseline obstructive spirometric patterns, experienced lower FEV1% and FEV1/FVC decline than non-RA comparators. Conversely, never smokers with RA had more FEV1% decline than non-RA comparators. Future studies should investigate potential treatments and the pathogenesis of obstructive lung diseases in smokers with RA.


Asunto(s)
Artritis Reumatoide , Fumar , Espirometría , Humanos , Artritis Reumatoide/diagnóstico , Artritis Reumatoide/fisiopatología , Masculino , Femenino , Persona de Mediana Edad , Estudios Longitudinales , Estudios Prospectivos , Fumar/efectos adversos , Fumar/epidemiología , Anciano , Volumen Espiratorio Forzado , Capacidad Vital , Enfermedad Pulmonar Obstructiva Crónica/fisiopatología , Enfermedad Pulmonar Obstructiva Crónica/epidemiología , Enfermedad Pulmonar Obstructiva Crónica/diagnóstico , Enfermedad Pulmonar Obstructiva Crónica/etiología , Adulto , Reino Unido/epidemiología
15.
Cells ; 13(11)2024 May 21.
Artículo en Inglés | MEDLINE | ID: mdl-38891017

RESUMEN

Telomeres, potential biomarkers of aging, are known to shorten with continued cigarette smoke exposure. In order to further investigate this process and its impact on cellular stress and inflammation, we used an in vitro model with cigarette smoke extract (CSE) and observed the downregulation of telomere stabilizing TRF2 and POT1 genes after CSE treatment. hTERT is a subunit of telomerase and a well-known oncogenic marker, which is overexpressed in over 85% of cancers and may contribute to lung cancer development in smokers. We also observed an increase in hTERT and ISG15 expression levels after CSE treatment, as well as increased protein levels revealed by immunohistochemical staining in smokers' lung tissue samples compared to non-smokers. The effects of ISG15 overexpression were further studied by quantifying IFN-γ, an inflammatory protein induced by ISG15, which showed greater upregulation in smokers compared to non-smokers. Similar changes in gene expression patterns for TRF2, POT1, hTERT, and ISG15 were observed in blood and buccal swab samples from smokers compared to non-smokers. The results from this study provide insight into the mechanisms behind smoking causing telomere shortening and how this may contribute to the induction of inflammation and/or tumorigenesis, which may lead to comorbidities in smokers.


Asunto(s)
Envejecimiento , Citocinas , Inflamación , Complejo Shelterina , Fumar , Telomerasa , Telómero , Proteína 2 de Unión a Repeticiones Teloméricas , Humanos , Inflamación/genética , Inflamación/patología , Envejecimiento/genética , Proteína 2 de Unión a Repeticiones Teloméricas/metabolismo , Proteína 2 de Unión a Repeticiones Teloméricas/genética , Citocinas/metabolismo , Telómero/metabolismo , Telomerasa/metabolismo , Telomerasa/genética , Fumar/efectos adversos , Ubiquitinas/metabolismo , Ubiquitinas/genética , Proteínas de Unión a Telómeros/metabolismo , Proteínas de Unión a Telómeros/genética , Interferón gamma/metabolismo , Homeostasis del Telómero , Masculino , Acortamiento del Telómero , Femenino , Persona de Mediana Edad
16.
Int J Mol Sci ; 25(11)2024 May 31.
Artículo en Inglés | MEDLINE | ID: mdl-38892256

RESUMEN

E-cigarette users predominantly also continue to smoke cigarettes. These Dual Users either consume e-cigarettes in locations where smoking is not allowed, but vaping is, or to reduce their consumption of cigarettes, believing it will lead to harm reduction. Whilst it is known that e-cigarette vapour is chemically less complex than cigarette smoke, it has a distinct chemical profile, and very little is known about the health impacts of exposure to both chemical profiles vs. either alone. We simultaneously exposed cells in vitro to non-toxic levels of e-cigarette vapour extract (EVE) and cigarette smoke extract (CSE) to determine their effects on 16HBE14o- airway epithelial cell metabolism and inflammatory response, as well as immune cell (THP-1 cells and monocyte-derived macrophages (MDM) from healthy volunteers) migration, phagocytosis, and inflammatory response. We observed increased toxicity, reduced metabolism (a marker of proliferation) in airway epithelial cells, and reduced monocyte migration, macrophage phagocytosis, and altered chemokine production after exposure to either CSE or EVE. These cellular responses were greater after dual exposure to CSE and EVE. The airway epithelial cells from smokers showed reduced metabolism after EVE (the Switcher model) and dual CSE and EVE exposure. When EVE and CSE were allowed to interact, the chemicals were found to be altered, and new chemicals were also found compared to the CSE and EVE profiles. Dual exposure to e-cigarette vapour and cigarette smoke led to worse functional outcomes in cells compared to either single exposure alone, adding to limited data that dual use may be more dangerous than smoking only.


Asunto(s)
Sistemas Electrónicos de Liberación de Nicotina , Macrófagos , Monocitos , Humanos , Macrófagos/metabolismo , Macrófagos/efectos de los fármacos , Monocitos/metabolismo , Monocitos/efectos de los fármacos , Humo/efectos adversos , Células Epiteliales/metabolismo , Células Epiteliales/efectos de los fármacos , Cigarrillo Electrónico a Vapor/efectos adversos , Vapeo/efectos adversos , Fagocitosis/efectos de los fármacos , Células THP-1 , Movimiento Celular/efectos de los fármacos , Fumar/efectos adversos , Productos de Tabaco/efectos adversos
17.
Clin Transl Med ; 14(6): e1733, 2024 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-38877637

RESUMEN

BACKGROUND AND AIMS: Smoking is recognised as an independent risk factor in the development of chronic pancreatitis (CP). Cystic fibrosis transmembrane conductance regulator (CFTR) function and ductal fluid and bicarbonate secretion are also known to be impaired in CP, so it is crucial to understand the relationships between smoking, pancreatic ductal function and the development of CP. METHODS: We measured sweat chloride (Cl-) concentrations in patients with and without CP, both smokers and non-smokers, to assess CFTR activity. Serum heavy metal levels and tissue cadmium concentrations were determined by mass spectrometry in smoking and non-smoking patients. Guinea pigs were exposed to cigarette smoke, and cigarette smoke extract (CSE) was prepared to characterise its effects on pancreatic HCO3 - and fluid secretion and CFTR function. We administered cerulein to both the smoking and non-smoking groups of mice to induce pancreatitis. RESULTS: Sweat samples from smokers, both with and without CP, exhibited elevated Cl- concentrations compared to those from non-smokers, indicating a decrease in CFTR activity due to smoking. Pancreatic tissues from smokers, regardless of CP status, displayed lower CFTR expression than those from non-smokers. Serum levels of cadmium and mercury, as well as pancreatic tissue cadmium, were increased in smokers. Smoking, CSE, cadmium, mercury and nicotine all hindered fluid and HCO3 - secretion and CFTR activity in pancreatic ductal cells. These effects were mediated by sustained increases in intracellular calcium ([Ca2+]i), depletion of intracellular ATP (ATPi) and mitochondrial membrane depolarisation. CONCLUSION: Smoking impairs pancreatic ductal function and contributes to the development of CP. Heavy metals, notably cadmium, play a significant role in the harmful effects of smoking. KEY POINTS: Smoking and cigarette smoke extract diminish pancreatic ductal fluid and HCO3 - secretion as well as the expression and function of CFTR Cd and Hg concentrations are significantly higher in the serum samples of smokers Cd accumulates in the pancreatic tissue of smokers.


Asunto(s)
Metales Pesados , Pancreatitis Crónica , Humanos , Pancreatitis Crónica/metabolismo , Pancreatitis Crónica/inducido químicamente , Animales , Metales Pesados/metabolismo , Masculino , Ratones , Femenino , Persona de Mediana Edad , Cobayas , Adulto , Conductos Pancreáticos/metabolismo , Conductos Pancreáticos/efectos de los fármacos , Regulador de Conductancia de Transmembrana de Fibrosis Quística/metabolismo , Fumar/efectos adversos , Fumar/metabolismo , Modelos Animales de Enfermedad
18.
Nutrients ; 16(11)2024 Jun 06.
Artículo en Inglés | MEDLINE | ID: mdl-38892724

RESUMEN

BACKGROUND AND PURPOSE: Diet might be a modifiable factor in preventing cancer by modulating inflammation. This study aims to explore the association between the dietary inflammatory index (DII) score and the risk of bladder cancer (BC). METHODS: A total of 112 BC patients and 292 control subjects were enrolled in a case-control trial. Additionally, we tracked a total of 109 BC patients and 319 controls, whose propensity scores were obtained from the Nutrition Examination Survey (NHANES) database spanning from 1999 to 2020. The baseline index and dietary intake data were assessed using a food frequency questionnaire (FFQ). DII scores were calculated based on the dietary intake of 20 nutrients obtained from participants and categorized into four groups. The association between the inflammatory potential of the diet and BC risk was investigated using multivariate odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: High DII scores were associated with a pro-inflammatory diet and a higher risk of BC, with higher DII scores positively associated with a higher risk of BC (quartiles 4 vs. 1, ORs 4.89, 95% CIs 2.09-11.25 p < 0.001). Specifically, this might promote BC development by inducing oxidative stress and affecting DNA repair mechanisms. This result was consistent with the NHANES findings (quartiles 4 vs. 1, ORs 2.69, 95% CIs 1.25-5.77, p = 0.006) and further supported the association of pro-inflammatory diet and lifestyle factors with the risk of BC. CONCLUSIONS: Diets with the highest pro-inflammatory potential were associated with an increased risk of BC. By adjusting lifestyle factors, individuals might effectively lower their DII, thereby reducing the risk of developing BC. The results are consistent with the NHANES cohort.


Asunto(s)
Consumo de Bebidas Alcohólicas , Dieta , Inflamación , Encuestas Nutricionales , Neoplasias de la Vejiga Urinaria , Humanos , Neoplasias de la Vejiga Urinaria/epidemiología , Neoplasias de la Vejiga Urinaria/prevención & control , Neoplasias de la Vejiga Urinaria/etiología , Masculino , Estudios de Casos y Controles , Femenino , Persona de Mediana Edad , Dieta/efectos adversos , Dieta/estadística & datos numéricos , Consumo de Bebidas Alcohólicas/efectos adversos , Consumo de Bebidas Alcohólicas/epidemiología , Factores de Riesgo , Fumar/efectos adversos , Fumar/epidemiología , Anciano , Oportunidad Relativa , Adulto
19.
Sci Rep ; 14(1): 14179, 2024 06 19.
Artículo en Inglés | MEDLINE | ID: mdl-38898083

RESUMEN

Exposures to social and environmental stressors arise individual behavioural response and thus indirectly affect cardiometabolic health. The aim of this study was to investigate several social and environmental stressors and the paths of their influence on cardiometabolic health. The data of 2154 participants (aged 25-64 years) from the cross-sectional population-based study were analysed. The composite score of metabolic disorders (MS score) was calculated based on 5 biomarkers: waist circumference, blood pressure, fasting blood glucose, HDL-cholesterol, triglycerides. The effects of social stressors (education level, income), environmental stressors (NO2, noise) and behavioural factors (unhealthy diet, smoking, alcohol consumption, sedentary behaviours) on MS score were assessed using a structural model. We observed a direct effect of education on MS score, as well as an indirect effect mediated via an unhealthy diet, smoking, and sedentary behaviours. We also observed a significant indirect effect of income via sedentary behaviours. The only environmental stressor predicting MS was noise, which also mediated the effect of education. In summary, the effect of social stressors on the development of cardiometabolic risk had a higher magnitude than the effect of the assessed environmental factors. Social stressors lead to an individual's unhealthy behaviour and might predispose individuals to higher levels of environmental stressors exposures.


Asunto(s)
Conducta Sedentaria , Humanos , Masculino , Persona de Mediana Edad , Adulto , Femenino , Estudios Transversales , Estrés Psicológico , Presión Sanguínea , Triglicéridos/sangre , Circunferencia de la Cintura , Glucemia/metabolismo , Enfermedades Metabólicas/etiología , Enfermedades Metabólicas/epidemiología , Fumar/efectos adversos , Exposición a Riesgos Ambientales/efectos adversos , Enfermedades Cardiovasculares/etiología , Enfermedades Cardiovasculares/epidemiología , HDL-Colesterol/sangre , Biomarcadores/sangre , Factores de Riesgo
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