cotinine/inflamație

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The relationship between cotinine concentrations and inflammatory markers among highly secondhand smoke exposed non-smoking adolescents.

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BACKGROUND Secondhand smoke (SHS) exposure is a risk factor of respiratory, cardiovascular and inflammatory diseases, however its association with inflammatory markers among highly SHS exposed adolescents has not yet been explored. METHODS Participants included in this study were a subset of 68

Association between smoking status assessed with plasma-cotinine and inflammatory and endothelial biomarkers in HIV-positive and HIV-negative individuals.

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OBJECTIVE Smoking is a major contributor to mortality and morbidity in HIV-positive individuals. Our primary objective was to evaluate the association between smoking status determined by plasma cotinine (P-cotinine) concentration and inflammatory and endothelial biomarkers in HIV-positive versus

Dose-Dependent Toxic Effect of Cotinine-Verified Tobacco Smoking on Systemic Inflammation in Apparently Healthy Men and Women: A Nationwide Population-Based Study.

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Chronic exposure to tobacco smoke leads to chronic low-grade systemic inflammation; however, little is known about the dose-dependent toxic effect of objective tobacco smoking on systemic inflammation. We examined the dose-dependent toxic effect of cotinine-verified tobacco smoking on leukocyte

Cotinine inhibits the pro-inflammatory response initiated by multiple cell surface Toll-like receptors in monocytic THP cells.

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BACKGROUND The primary, stable metabolite of nicotine [(S)-3-(1-methyl-2-pyrrolidinyl) pyridine] in humans is cotinine [(S)-1-methyl-5-(3-pyridinyl)-2-pyrrolidinone]. We have previously shown that cotinine exposure induces convergence and amplification of the GSK3β-dependent PI3 kinase and

Cotinine-induced convergence of the cholinergic and PI3 kinase-dependent anti-inflammatory pathways in innate immune cells.

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Nicotine [(S)-3-(1-methyl-2-pyrrolidinyl)pyridine] is a major component of tobacco and a highly efficient acetylcholine receptor (nAChR) agonist that triggers the cholinergic anti-inflammatory pathway. We demonstrate that pre-treatment of monocytes with the stable nicotine catabolite, cotinine

Cotinine aggravates inflammatory response in thromboangiitis obliterans through TLR-4/MyD88/NF-κB inflammatory signaling pathway.

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Clinical and radiographic periodontal status and whole salivary cotinine, IL-1β and IL-6 levels in cigarette- and waterpipe-smokers and E-cig users.

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The aim was to compare the clinical (plaque index [PI], bleeding on probing [BOP], probing pocket depth [PPD] and clinical attachment loss [CAL]) and radiographic (marginal bone loss [MBL]) periodontal parameters and whole salivary cotinine, interleukin (IL)-1β and IL-6 levels among

Secondhand smoke exposure and inflammatory markers in nonsmokers in the trucking industry.

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BACKGROUND Few studies have directly assessed the association of secondhand smoke (SHS) with cardiovascular disease-related inflammatory markers, and the findings are inconsistent. OBJECTIVE We assessed the association between SHS exposure and the inflammatory markers high-sensitivity C-reactive

Effects of maternal inflammation and exposure to cigarette smoke on birth weight and delivery of preterm babies in a cohort of indigenous Australian women.

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Sudden infant death syndrome (SIDS), neonatal deaths, and deaths from infection are higher among Indigenous Australians. This study aimed to determine the effects of inflammatory responses and exposure to cigarette smoke, two important factors associated with sudden death in infancy, on preterm

Objectively measured secondhand smoke exposure and risk of cardiovascular disease: what is the mediating role of inflammatory and hemostatic factors?

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OBJECTIVE The aim of this study was to examine the association between objectively measured secondhand smoke (SHS) exposure and incident cardiovascular disease (CVD) death and assess the extent to which this association can be explained through novel circulating markers of inflammation and

Inflammatory activation and cholinergic anti-inflammatory system in eating disorders.

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Dysfunctional serotoninergic regulation and hypothalamic-pituitary-adrenal (HPA) axis overreactivity have been consistently reported in research studies with eating disorders (ED). In addition, the links between stress response, serotonin function, HPA axis and inflammatory mechanisms in ED have

Relationships between cotinine, lower respiratory tract infection, and eosinophil cationic protein in children.

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BACKGROUND The aim of this study was to investigate the effect of passive smoking on urine eosinophil cationic protein (u-ECP) in children with lower respiratory tract infections (LRTI). METHODS This was a case-control study. The study cohort consisted of 150 children with LRTI (case group) and 150

Low grade inflammation and ECG left ventricular hypertrophy in urban African males: The SABPA study.

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BACKGROUND Hypertension and vascular hyperresponsiveness have been associated with structural wall abnormalities in black Africans. Whether low grade inflammation would have an additive effect is uncertain. Therefore, a novel investigation aimed to assess whether inflammation and pressure overload

The interactions between cigarette smoking and reduced lung function on systemic inflammation.

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BACKGROUND Low-grade systemic inflammation is commonly observed in conditions associated with reduced FEV(1). Active cigarette smoking, which is a leading risk factor for decreased FEV(1), can also independently induce systemic inflammation. OBJECTIVE To determine the independent contributions of

Sudden infant death syndrome: postmortem findings of nicotine and cotinine in pericardial fluid of infants in relation to morphological changes and position at death.

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Parental smoking is considered to be an important risk factor for the sudden infant death syndrome (SIDS). We studied the concentrations of nicotine and cotinine in the pericardial fluid of SIDS and non-SIDS victims, with particular emphasis on the relationship to body position at the time of death

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