scholarly journals Trace Elements in Urban Particulate Matters: Variations in Serum Levels, Inhalation Bioaccessibility, Health and Disease Effects

2021 ◽  
Author(s):  
Emmanuel Gbenga Olumayede ◽  
B. Babalola ◽  
I. Oghenovo
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Trace Elements ◽  
Idiopathic Pulmonary Fibrosis ◽  
Serum Levels ◽  
Chronic Obstructive ◽  
Particulate Matters ◽  
Obstructive Pulmonary Disease ◽  
Health And Disease ◽  
Simulated Body Fluids ◽  
Ntm Lung Disease

Trace elements-bound to particulate matters are often become entrained in human respiratory airway, deposited in human nasal cavity and made available for absorption by human tracheobronchial. It has been assumed that variability and bioaccessibility of elements in the serum correlate with some health and diseases. This chapter is a summary of previous works on bioaccessibility of trace elements bound to inhale particulates using different kinds of simulated body fluids. Presented also are evidences of serum variation in some respiratory diseases, such as chronic obstructive pulmonary disease (with or without hypertension), emphysema, bronchiectasis and bronchial asthma, non-tuberculose mycobacterial (NTM) lung disease, idiopathic pulmonary fibrosis (IPF).

Oxidized low-density lipoproteins and its connection with dyslipidemia, inflammatory markers, and oxidative stress in patients with occupational chronic obstructive pulmonary disease

2021 ◽  
Vol 31 (4) ◽  
pp. 456-462
Author(s):  
I. A. Umnyagina ◽  
L. A. Strakhova ◽  
T. V. Blinova ◽  
V. V. Troshin ◽  
V. D. Fedotov
Keyword(s):  
Oxidative Stress ◽  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Comparison Group ◽  
Serum Levels ◽  
Low Density Lipoproteins ◽  
Chronic Obstructive ◽  
Low Density ◽  
Obstructive Pulmonary Disease ◽  
Occupational Copd

The role of low-density oxidized lipoproteins (OxLDL) in the pathogenesis of occupational chronic obstructive pulmonary disease (COPD) is not understood well enough.The study aims to determine the serum levels of oxidized low-density lipoproteins and their relationship with lipid profile, the level of oxidative stress and level C-reactive protein in patients with occupational chronic obstructive pulmonary disease.Methods. 116 patients diagnosed with occupational COPD and 25 patients with no respiratory diseases (comparison group) were examined. Serum levels of OxLDL was determined by solid phase enzyme-linked immunosorbent assay (ELISA) using the commercial reagent kit MDA-oxLDL from Biomedica Gruppe, Austria.Results. Circulating OxLDL was detected in serum in a significant proportion of patients with stable occupational COPD. In most of the patients, the concentration of OxLDL was within the values observed in the comparison group or exceeded them by no more than two times. In the minority of patients with occupational COPD (16.5%), the concentration of OxLDL was high and 4 – 10 times higher than its average value in the comparison group. It can be assumed that the revealed differences in the concentration of OxLDL are due to the different degree and intensity of oxidation of low-density lipoproteins. The relationships between OxLDL and lipid metabolism, oxidative stress (OS), the antioxidant capacity of serum (AOS), and serum levels of C-reactive protein were described.Conclusion. Serum OxLDL levels in patients with occupational COPD, the relationship between OxLDL and lipid metabolism, oxidative stress, and inflammation will provide an expanded view of the pathogenetic aspects of occupational COPD.

scholarly journals Association between ambient fine particulate matters and chronic obstructive pulmonary disease (COPD) mortality: an analysis in Southeastern China

2020 ◽  
Author(s):  
Zhijian Chen ◽  
Qiuli Fu ◽  
Guangming Mao ◽  
Lizhi Wu ◽  
Peiwei Xu ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Mixed Model ◽  
Fine Particles ◽  
Chronic Obstructive ◽  
Particulate Matters ◽  
Southeastern China ◽  
Obstructive Pulmonary Disease ◽  
Adverse Health Effects ◽  
Copd Mortality

Abstract Background: The objective of this study was to investigate the association between ambient particulate matters(PMs)and chronic obstructive pulmonary disease (COPD) mortality.Methods: Generalized Additive Mixed Model was employed to investigate the effects of ambient fine and coarse PMs on COPD mortality using 13,066 deaths from 2014 to 2016 among six cities in Zhejiang Province in Southeastern China.Results: The daily average death count due to COPD was 3, varying from 1 to 7among six cities. The daily 24-hour mean concentrations were diverse among cities, from 29.7 to 56.8 µg/m3 for PM2.5, 16.7 to 30.3 µg/m3 for PM2.5−10, and 50.3 to 87.1 µg/m3 for PM10, respectively. The analysis showed that daily exposure to PM2.5 and PM10 was associated with increased mortality due to COPD and that weak effects were observed between PM2.5−10 and COPD mortality.Conclusions: Our results provided evidence that the fine particles in air pollution have stronger functions on adverse health effects other than coarser particles in Southeastern China, which may be considered as a potential clinic target in PM-associated COPD.

scholarly journals Non-coding RNAs as Regulators of Cellular Senescence in Idiopathic Pulmonary Fibrosis and Chronic Obstructive Pulmonary Disease

2020 ◽  
Vol 7 ◽  
Author(s):  
Norihito Omote ◽  
Maor Sauler
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Pulmonary Disease ◽  
Cell Fate ◽  
Cellular Senescence ◽  
Cellular Stress ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Non Coding Rnas

Cellular senescence is a cell fate implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD). Cellular senescence occurs in response to cellular stressors such as oxidative stress, DNA damage, telomere shortening, and mitochondrial dysfunction. Whether these stresses induce cellular senescence or an alternative cell fate depends on the type and magnitude of cellular stress, but also on intrinsic factors regulating the cellular stress response. Non-coding RNAs, including both microRNAs and long non-coding RNAs, are key regulators of cellular stress responses and susceptibility to cellular senescence. In this review, we will discuss cellular mechanisms that contribute to senescence in IPF and COPD and highlight recent advances in our understanding of how these processes are influenced by non-coding RNAs. We will also discuss the potential therapeutic role for targeting non-coding RNAs to treat these chronic lung diseases.

scholarly journals Changes in Th1/Th2-producing cytokines during acute exacerbation chronic obstructive pulmonary disease

2018 ◽  
Vol 46 (9) ◽  
pp. 3890-3902 ◽  
Author(s):  
Bing Wei ◽  
Chun Sheng Li
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Acute Exacerbation ◽  
Chronic Obstructive Lung Disease ◽  
Serum Levels ◽  
T Cell Subsets ◽  
Th2 Cells ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Ifn Γ

Objective This study aimed to explore cytokine serum levels and the ratio of type 1 T helper (Th1)/Th2 cells in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). Methods A total 245 patients diagnosed with AECOPD and 193 patients who progressed to stable COPD after the initiation of treatment in hospital were selected, while a further 50 healthy individuals served as controls. All patients with COPD were diagnosed using Global Initiative for Chronic Obstructive Lung Disease criteria. Serum concentrations of interleukin (IL)-2, interferon (IFN)-γ, IL-4, IL-10, IL-17, and immunoglobulin (Ig)E were measured using enzyme-linked immunosorbent assays. Results AECOPD patients had higher levels of IL-2, IFN-γ, IL-4, IL-10, IL-17, and IgE than those with stable COPD or controls. Intriguingly, the ratios of Th1/Th2 and IL-17/IgE were lower in AECOPD patients compared with the other two groups. These data suggest that AECOPD patients produce more IgE and have more differentiated Th2 cells than other groups. Conclusion Our findings suggest that an imbalance of circulating CD4+ T cell subsets correlates with AECOPD, and that a shift of Th1/Th2 and IL-17/IgE ratios may be caused by increased Th2 cell production.

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