Systemic profiles of micrornas, redox balance, and inflammation in lung cancer patients : influence of copd

Altres ajuts: This study has been supported by Spanish Ministry of Science and Innovation, Sociedad Española de Neumología y Cirugía Torácica (SEPAR) 2018 & 2020.Lung cancer (LC) risk increases in patients with chronic respiratory diseases (COPD). MicroRNAs and redox imbalance are involved in lung tumorigenesis in COPD patients. Whether systemic alterations of those events may also take place in LC patients remains unknown. Our objectives were to assess the plasma levels of microRNAs, redox balance, and cytokines in LC patients with/without COPD. MicroRNAs (RT-PCR) involved in LC, oxidized DNA, MDA-protein adducts, GSH, TEAC, VEGF, and TGF-beta (ELISA) were quantified in plasma samples from non-LC controls (n = 45), LC-only patients (n = 32), and LC-COPD patients (n = 91). In LC-COPD patients compared to controls and LC-only, MDA-protein adduct levels increased, while those of GSH decreased, and two patterns of plasma microRNA were detected. In both LC patient groups, miR-451 expression was downregulated, while those of microRNA-let7c were upregulated, and levels of TEAC and TGF-beta increased compared to the controls. Correlations were found between clinical and biological variables. A differential expression profile of microRNAs was detected in patients with LC. Moreover, in LC patients with COPD, plasma oxidative stress levels increased, whereas those of GSH declined. Systemic oxidative and antioxidant markers are differentially expressed in LC patients with respiratory diseases, thus implying its contribution to the pathogenesis of tumorigenesis in these patients

Resveratrol Ameliorates Cardiac Remodeling in a Murine Model of Heart Failure With Preserved Ejection Fraction

Objective: Accumulating evidence suggested that resveratrol (RES) could protect against adverse cardiac remodeling induced by several cardiovascular diseases. However, the role of RES in the setting of heart failure with preserved ejection fraction (HFpEF) and the underlying mechanisms of its action remain understood. This study was to determine whether RES could ameliorate HFpEF-induced cardiac remodeling and its mechanisms.Methods:In vivo, C57BL/6 mice served as either the sham or the HFpEF model. The HFpEF mice model was induced by uninephrectomy surgery and d-aldosterone infusion. RES (10 mg/kg/day, ig) or saline was administered to the mice for four weeks. In vitro, transforming growth factor β1 (TGF-β1) was used to stimulate neonatal rat cardiac fibroblasts (CFs) and Ex-527 was used to inhibit sirtuin 1 (Sirt1) in CFs. Echocardiography, hemodynamics, western blotting, quantitative real-time PCR, histological analysis, immunofluorescence, and ELISA kits were used to evaluate cardiac remodeling induced by HFpEF. Sirt1 and Smad3 expressions were measured to explore the underlying mechanisms of RES.Results: HFpEF mice developed left ventricular hypertrophy, preserved ejection fraction, diastolic dysfunction, and pulmonary congestion. Moreover, HFpEF mice showed increased infiltration of neutrophils and macrophages into the heart, including increased interleukin (IL)-1β, IL-6, and TNF-α. We also observed elevated M1 macrophages and decreased M2 macrophages, which were exhibited by increased mRNA expression of M1 markers (iNOS, CD86, and CD80) and decreased mRNA expression of M2 markers (Arg1, CD163, and CD206) in HFpEF hearts. Moreover, HFpEF hearts showed increased levels of intracellular reactive oxygen species (ROS). Importantly, HFpEF mice depicted increased collagen-I and -III and TGF-β mRNA expressions and decreased protein expression of phosphorylated endothelial nitric-oxide synthase (p-eNOS). Results of western blot revealed that the activated TGF-β/Smad3 signaling pathway mediated HFpEF-induced cardiac remodeling. As expected, this HFpEF-induced cardiac remodeling was reversed when treated with RES. RES significantly decreased Smad3 acetylation and inhibited Smad3 transcriptional activity induced by HFpEF via activating Sirt1. Inhibited Sirt1 with Ex-527 increased Smad3 acetylation, enhanced Smad3 transcriptional activity, and offset the protective effect of RES on TGF-β–induced cardiac fibroblast–myofibroblast transformation in CFs.Conclusion: Our results suggested that RES exerts a protective action against HFpEF-induced adverse cardiac remodeling by decreasing Smad3 acetylation and transcriptional activity via activating Sirt1. RES is expected to be a novel therapy option for HFpEF patients

Identification of necroptosis-related genes in Parkinson’s disease by integrated bioinformatics analysis and experimental validation

BackgroundParkinson’s disease (PD) is the second most common neurodegeneration disease worldwide. Necroptosis, which is a new form of programmed cell death with high relationship with inflammation, plays a vital role in the progression of PD. However, the key necroptosis related genes in PD are not fully elucidated.PurposeIdentification of key necroptosis-related genes in PD.MethodThe PD associated datasets and necroptosis related genes were downloaded from the GEO Database and GeneCards platform, respectively. The DEGs associated with necroptosis in PD were obtained by gap analysis, and followed by cluster analysis, enrichment analysis and WGCNA analysis. Moreover, the key necroptosis related genes were generated by PPI network analysis and their relationship by spearman correlation analysis. Immune infiltration analysis was used for explore the immune state of PD brain accompanied with the expression levels of these genes in various types of immune cells. Finally, the gene expression levels of these key necroptosis related genes were validated by an external dataset, blood samples from PD patients and toxin-induced PD cell model using real-time PCR analysis.ResultTwelve key necroptosis-related genes including ASGR2, CCNA1, FGF10, FGF19, HJURP, NTF3, OIP5, RRM2, SLC22A1, SLC28A3, WNT1 and WNT10B were identified by integrated bioinformatics analysis of PD related dataset GSE7621. According to the correlation analysis of these genes, RRM2 and WNT1 were positively and negatively correlated with SLC22A1 respectively, while WNT10B was positively correlated with both OIF5 and FGF19. As the results from immune infiltration analysis, M2 macrophage was the highest population of immune cell in analyzed PD brain samples. Moreover, we found that 3 genes (CCNA1, OIP5 and WNT10B) and 9 genes (ASGR2, FGF10, FGF19, HJURP, NTF3, RRM2, SLC22A1, SLC28A3 and WNT1) were down- and up- regulated in an external dataset GSE20141, respectively. All the mRNA expression levels of these 12 genes were obviously upregulated in 6-OHDA-induced SH-SY5Y cell PD model while CCNA1 and OIP5 were up- and down- regulated, respectively, in peripheral blood lymphocytes of PD patients.ConclusionNecroptosis and its associated inflammation play fundamental roles in the progression of PD and these identified 12 key genes might be served as new diagnostic markers and therapeutic targets for PD

Molecular Characteristics of Staphylococcus aureus From Food Samples and Food Poisoning Outbreaks in Shijiazhuang, China

As an opportunistic pathogen worldwide, Staphylococcus aureus can cause food poisoning and human infections. This study investigated the sequence typing, the penicillin (blaZ) and methicillin (mec) resistance profiles of S. aureus from food samples and food poisoning outbreaks in Shijiazhuang City, and the staphylococcal enterotoxin (SE) types of the S. aureus isolates from food poisoning. A total of 138 foodborne S. aureus isolates were distributed into 8 clonal complexes (CCs) and 12 singletons. CC1, CC5, CC8, CC15, CC97, CC59, CC398, CC88, and CC7 were the predominant CCs of foodborne S. aureus isolates. Moreover, CC59, CC15, and CC5 were the most prevalent CCs in food poisoning outbreaks. SEE was the most commonly detected SE in food poisoning isolates. One hundred thirty-three S. aureus isolates harbored the penicillin-resistant gene blaZ, and nine isolates carried the mec gene. The present study further explained the relationship between S. aureus and foods and food poisoning and indicated the potential risk of S. aureus infection

A highly selective fluorogenic probe for the detection and in vivo imaging of Cu/Zn superoxide dismutase

Copper/zinc superoxide dismutase (Cu/Zn SOD) is an essential enzyme that protects tissue from oxidative damage. Herein we report the first fluorogenic probe (SODO) for the detection and in vivo imaging of Cu/Zn SOD. SODO represents a unique chemical probe for translational imaging studies of Cu/Zn SOD in inflammatory disorders.1110sciescopu

Actively implementing an evidence-based feeding guideline for critically ill patients (NEED): a multicenter, cluster-randomized, controlled trial

Background: Previous cluster-randomized controlled trials evaluating the impact of implementing evidence-based guidelines for nutrition therapy in critical illness do not consistently demonstrate patient benefits. A large-scale, sufficiently powered study is therefore warranted to ascertain the effects of guideline implementation on patient-centered outcomes. Methods: We conducted a multicenter, cluster-randomized, parallel-controlled trial in intensive care units (ICUs) across China. We developed an evidence-based feeding guideline. ICUs randomly allocated to the guideline group formed a local "intervention team", which actively implemented the guideline using standardized educational materials, a graphical feeding protocol, and live online education outreach meetings conducted by members of the study management committee. ICUs assigned to the control group remained unaware of the guideline content. All ICUs enrolled patients who were expected to stay in the ICU longer than seven days. The primary outcome was all-cause mortality within 28 days of enrollment. Results: Forty-eight ICUs were randomized to the guideline group and 49 to the control group. From March 2018 to July 2019, the guideline ICUs enrolled 1399 patients, and the control ICUs enrolled 1373 patients. Implementation of the guideline resulted in significantly earlier EN initiation (1.20 vs. 1.55 mean days to initiation of EN; difference − 0.40 [95% CI − 0.71 to − 0.09]; P = 0.01) and delayed PN initiation (1.29 vs. 0.80 mean days to start of PN; difference 1.06 [95% CI 0.44 to 1.67]; P = 0.001). There was no significant difference in 28-day mortality (14.2% vs. 15.2%; difference − 1.6% [95% CI − 4.3% to 1.2%]; P = 0.42) between groups. Conclusions: In this large-scale, multicenter trial, active implementation of an evidence-based feeding guideline reduced the time to commencement of EN and overall PN use but did not translate to a reduction in mortality from critical illness. Trial registration: ISRCTN, ISRCTN12233792. Registered November 20th, 2017

Actively implementing an evidence-based feeding guideline for critically ill patients (NEED): a multicenter, cluster-randomized, controlled trial.

BackgroundPrevious cluster-randomized controlled trials evaluating the impact of implementing evidence-based guidelines for nutrition therapy in critical illness do not consistently demonstrate patient benefits. A large-scale, sufficiently powered study is therefore warranted to ascertain the effects of guideline implementation on patient-centered outcomes.MethodsWe conducted a multicenter, cluster-randomized, parallel-controlled trial in intensive care units (ICUs) across China. We developed an evidence-based feeding guideline. ICUs randomly allocated to the guideline group formed a local "intervention team", which actively implemented the guideline using standardized educational materials, a graphical feeding protocol, and live online education outreach meetings conducted by members of the study management committee. ICUs assigned to the control group remained unaware of the guideline content. All ICUs enrolled patients who were expected to stay in the ICU longer than seven days. The primary outcome was all-cause mortality within 28 days of enrollment.ResultsForty-eight ICUs were randomized to the guideline group and 49 to the control group. From March 2018 to July 2019, the guideline ICUs enrolled 1399 patients, and the control ICUs enrolled 1373 patients. Implementation of the guideline resulted in significantly earlier EN initiation (1.20 vs. 1.55 mean days to initiation of EN; difference - 0.40 [95% CI - 0.71 to - 0.09]; P = 0.01) and delayed PN initiation (1.29 vs. 0.80 mean days to start of PN; difference 1.06 [95% CI 0.44 to 1.67]; P = 0.001). There was no significant difference in 28-day mortality (14.2% vs. 15.2%; difference - 1.6% [95% CI - 4.3% to 1.2%]; P = 0.42) between groups.ConclusionsIn this large-scale, multicenter trial, active implementation of an evidence-based feeding guideline reduced the time to commencement of EN and overall PN use but did not translate to a reduction in mortality from critical illness.Trial registrationISRCTN, ISRCTN12233792 . Registered November 20th, 2017

Actively implementing an evidence-based feeding guideline for critically ill patients (NEED): a multicenter, cluster-randomized, controlled trial (vol 26, 46, 2022)

BackgroundPrevious cluster-randomized controlled trials evaluating the impact of implementing evidence-based guidelines for nutrition therapy in critical illness do not consistently demonstrate patient benefits. A large-scale, sufficiently powered study is therefore warranted to ascertain the effects of guideline implementation on patient-centered outcomes.MethodsWe conducted a multicenter, cluster-randomized, parallel-controlled trial in intensive care units (ICUs) across China. We developed an evidence-based feeding guideline. ICUs randomly allocated to the guideline group formed a local "intervention team", which actively implemented the guideline using standardized educational materials, a graphical feeding protocol, and live online education outreach meetings conducted by members of the study management committee. ICUs assigned to the control group remained unaware of the guideline content. All ICUs enrolled patients who were expected to stay in the ICU longer than seven days. The primary outcome was all-cause mortality within 28 days of enrollment.ResultsForty-eight ICUs were randomized to the guideline group and 49 to the control group. From March 2018 to July 2019, the guideline ICUs enrolled 1399 patients, and the control ICUs enrolled 1373 patients. Implementation of the guideline resulted in significantly earlier EN initiation (1.20 vs. 1.55 mean days to initiation of EN; difference - 0.40 [95% CI - 0.71 to - 0.09]; P = 0.01) and delayed PN initiation (1.29 vs. 0.80 mean days to start of PN; difference 1.06 [95% CI 0.44 to 1.67]; P = 0.001). There was no significant difference in 28-day mortality (14.2% vs. 15.2%; difference - 1.6% [95% CI - 4.3% to 1.2%]; P = 0.42) between groups.ConclusionsIn this large-scale, multicenter trial, active implementation of an evidence-based feeding guideline reduced the time to commencement of EN and overall PN use but did not translate to a reduction in mortality from critical illness.Trial registrationISRCTN, ISRCTN12233792 . Registered November 20th, 2017

Role of inflammation and oxidative stress in the systemic manifestations of chronic respiratory diseases : lung cancer, chronic obstructive pulmonary disease, and bronchiectasis

Introducció: Les malalties respiratòries cròniques com el càncer de pulmó (CP), la malaltia pulmonar obstructiva crònica (MPOC) i les bronquiectàsies afecten tant les estructures pulmonars com els òrgans fora del sistema respiratori, com els ossos, els músculs, el cor i el compartiment sanguini. Les manifestacions sistèmiques en les malalties respiratòries cròniques són tan rellevants com les locals (respiratòries). Diversos mecanismes biològics, com ara el desequilibri redox, la inflamació i els microARNs, poden estar involucrats en la patogènia de les manifestacions sistèmiques en les malalties respiratòries cròniques. Hipòtesi: L'estrès oxidatiu, la inflamació, i els microARNs poden expressar-se diferencialment en el compartiment sistèmic (sang) dels pacients amb diferents malalties respiratòries: MPOC, bronquiectàsies no fibrosi quística (FQ), CP amb i sense MPOC. Objectius: En pacients amb CP i controls sense CP: 1) Avaluar els nivells plasmàtics de marcadors prooxidants, antioxidants i marcadors inflamatoris, i l'expressió de microARN potencialment implicats en la carcinogènesi pulmonar de pacients amb CP amb i sense MPOC, i controls sense CP; 2) Explorar associacions potencials entre variables biològiques i clíniques de pacients amb CP amb i sense MPOC. En pacients amb bronquiectàsies no FQ i controls sans: 1) Analitzar els nivells plasmàtics de cèl·lules i molècules inflamatòries, marcadors prooxidants i antioxidants en pacients amb bronquiectàsies no FQ i controls sans; 2) Avaluar les relacions entre variables biològiques i clíniques de pacients amb bronquiectàsies no FQ. Mètodes: S'obtingueren mostres de sang de tots els subjectes de l'estudi: 1) 32 pacients amb CP, 91 pacients amb CP-MPOC i 45 subjectes de control sense CP, i 2) 30 pacients amb bronquiectàsies no FQ i 26 controls sans. Es van analitzar la composició corporal, la funció pulmonar i els paràmetres sanguinis a tots els subjectes de tots els estudis. Anàlisi biològica: es va utilitzar ELISA per avaluar l'estrès oxidatiu i els marcadors d'inflamació als dos estudis. qRT-PCR es va utilitzar per analitzar els microARNs en pacients amb CP i controls sense CP. Resultats: 1) En els pacients amb CP en comparació dels controls sense CP, els nivells plasmàtics de glutatió reduït (GSH), la capacitat antioxidant equivalent al trolox (TEAC), el factor de creixement transformant beta1 (TGF-beta1) i l'expressió de microARNs (miR)-let7c van augmentar significativament, mentre que els de miR-451 van disminuir significativament; 2) Pacients amb CP-MPOC en comparació amb controls sense CP, els nivells plasmàtics d'adductes proteics de malondialdehid (MDA), TEAC, TGF-beta1 i l'expressió de miR-let7c van ser significativament més alts, mentre que els de GSH i de miR-451 van disminuir significativament; 3) En pacients amb CP-MPOC, els nivells plasmàtics de MDA van ser significativament més alts, mentre que els de GSH i de miR-210 van disminuir significativament en comparació dels pacients amb CP; 4) En pacients amb bronquiectàsies no FQ, els nivells de MDA, GSH, mieloperoxidasa, proteïna C reactiva, velocitat de sedimentació globular, fibrinogen, alfa-1 antitripsina, immunoglobulina (Ig) A i IgG van ser significativament més alts en comparació dels controls sans. Conclusions: Els marcadors oxidants i antioxidants sistèmics com MDA i GSH s'expressen de manera diferent en pacients amb CP-MPOC, contribuint així a la patogènia tumoral d'aquests pacients. Les bronquièctasies no FQ, per altra banda, van mostrar un augment en el nivell dels marcadors oxidants i antioxidants analitzats. La inflamació sistèmica té lloc al plasma de pacients amb CP i pacients amb bronquièctasies no FQ; aquestes troballes suggereixen que la inflamació pot estar involucrada en la patogènia d'aquestes malalties respiratòries cròniques. S'ha demostrat que els miARNs plasmàtics expressen de manera diferent en pacients amb CP, específicament miR-451, miR-let 7c i miR-210; suggerint que aquests miARNs poden ser marcadors crucials de la tumorigènesi pulmonar que podrien ajudar els pacients en la pràctica clínica.Introducción: Las enfermedades respiratorias crónicas como el cáncer de pulmón (CP), la enfermedad pulmonar obstructiva crónica (EPOC) y las bronquiectasias afectan tanto a las estructuras pulmonares como a órganos fuera del sistema respiratorio, como los huesos, los músculos, el corazón y el compartimento sanguíneo. Las manifestaciones sistémicas son tan relevantes como las locales (respiratorias) en las enfermedades respiratorias crónicas. Varios mecanismos biológicos, como el desequilibrio redox, la inflamación y los microARNs, pueden estar involucrados en la patogenia de las manifestaciones sistémicas en las enfermedades respiratorias crónicas. Hipótesis: El estrés oxidativo, inflamación, y microARNs pueden expresarse diferencialmente en el compartimento sistémico (sangre) de pacientes con diferentes enfermedades respiratorias: EPOC, bronquiectasias no fibrosis quística (FQ), CP con y sin EPOC. Objetivos: En pacientes con CP y controles sin CP: 1) Evaluar los niveles plasmáticos de marcadores prooxidantes, antioxidantes y marcadores inflamatorios, y la expresión de microARNs potencialmente implicados en la carcinogénesis pulmonar de pacientes con CP con y sin EPOC, y controles sin CP. 2) Explorar asociaciones potenciales entre variables biológicas y clínicas de pacientes con CP con y sin EPOC. En pacientes con bronquiectasias no FQ y controles sanos: 1) Analizar los niveles plasmáticos de células y moléculas inflamatorias, marcadores prooxidantes y antioxidantes de pacientes con bronquiectasias no FQ y controles sanos. 2) Evaluar las relaciones entre variables biológicas y clínicas de pacientes con bronquiectasias no FQ. Métodos: Se obtuvieron muestras de sangre de todos los sujetos del estudio: 1) 32 pacientes con CP, 91 pacientes con CP-EPOC y 45 sujetos de control sin CP, y 2) 30 pacientes con bronquiectasias no FQ y 26 controles sanos. Se analizaron la composición corporal, la función pulmonar y los parámetros sanguíneos en todos los sujetos de todos los estudios. Análisis biológico: se utilizó ELISA para evaluar el estrés oxidativo y los marcadores de inflamación en ambos estudios. qRT-PCR se utilizó para analizar los microARNs en pacientes con CP y controles sin CP. Resultados: 1) En los pacientes con CP en comparación con los controles sin CP, los niveles plasmáticos de glutatión reducido (GSH), la capacidad antioxidante equivalente al trolox (TEAC), el factor de crecimiento transformante beta1 (TGF-beta1) y la expresión de microARNs (miR)-let7c aumentaron significativamente, mientras que los de miR-451 disminuyeron significativamente. 2) Pacientes con CP-EPOC en comparación con controles sin CP, los niveles plasmáticos de aductos de proteína malondialdehído (MDA), TEAC, TGF-beta1 y la expresión de miR-let7c fueron significativamente más altos, mientras que los de GSH y de miR-451 disminuyeron significativamente. 3) En pacientes con CP-EPOC, los niveles plasmáticos de MDA fueron significativamente más altos, mientras que los de GSH y de miR-210 disminuyeron significativamente en comparación con los pacientes con CP. 4) En pacientes con bronquiectasias no FQ, los niveles de MDA, GSH, mieloperoxidasa, proteína C reactiva, velocidad de sedimentación globular, fibrinógeno, alfa-1 antitripsina, inmunoglobulina (Ig) A e IgG fueron significativamente más altos en comparación con los controles sanos. Conclusiones: Los marcadores oxidantes y antioxidantes sistémicos como MDA y GSH se expresan de forma diferente en pacientes con CP-EPOC, contribuyendo así a la patogenia tumoral de estos pacientes. Las bronquiectasias no FQ, por otro lado, mostraron un aumento en el nivel de los marcadores oxidantes y antioxidantes analizados. La inflamación sistémica tiene lugar en el plasma de pacientes con CP y pacientes con bronquiectasias no FQ; estos hallazgos sugieren que la inflamación puede estar involucrada en la patogenia de estas enfermedades respiratorias crónicas. Se ha demostrado que los miARNs plasmáticos expresan de manera diferente en pacientes con CP, específicamente miR-451, miR-let 7c y miR-210; sugiere que esos miARNs pueden ser marcadores cruciales de la tumorigénesis pulmonar que podrían ayudar a los pacientes en las práticas clínicas.Background: Chronic respiratory diseases such as lung cancer (LC), chronic obstructive pulmonary disease (COPD), and bronchiectasis affect both lung structures and organs beyond the respiratory system such as bones, muscles, heart, and blood compartment. Systemic manifestations are as relevant as local (respiratory) in chronic respiratory diseases. Several biological mechanisms such as redox imbalance, inflammation, and microRNAs may be involved in the pathogenesis of systemic manifestation in chronic respiratory diseases. Hypothesis: Oxidative stress, inflammation, and microRNAs may be differentially expressed in the systemic compartment (blood) of patients with different respiratory diseases: COPD, non-CF bronchiectasis, LC with and without COPD. Objectives: In LC patients and non-LC controls: 1) To evaluate plasma levels of prooxidants, antioxidants, inflammatory markers, and the expression of microRNAs potentially involved in lung carcinogenesis of LC patients with and without COPD and non-LC controls. 2) To explore potential associations between biological and clinical variables of LC patients with and without COPD. In bronchiectasis patients and healthy controls: 1) To analyze plasma levels of inflammatory cells and molecules, prooxidants, and antioxidants of non-CF bronchiectasis patients and healthy controls. 2) To assess the relationships between biological and clinical variables of non-CF bronchiectasis patients. Methods: Blood samples were obtained from all the study subjects: 1) 32 LC-only patients, 91 LC-COPD patients, and 45 non-LC control subjects, and 2) 30 non-CF bronchiectasis patients and 26 healthy controls. Body composition, lung function, and blood parameters were analyzed in all study subjects of all the studies. Biological analysis: ELISA was used to assess the oxidative stress and inflammation markers in both studies. qRT-PCR was used to analyze microRNAs in LC patients and non-LC controls. Results: 1) In LC-only patients compared to non-LC controls, plasma levels of GSH, TEAC, TGF-beta1, and the expression of miR-let7c were significantly increased, while those of miR-451 was significantly decreased. 2) In LC-COPD patients compared to non-LC controls, plasma levels of MDA-protein adducts, TEAC, TGF-beta1 and the expression of miR-let7c were significantly higher, while those of GSH and the expression of miR-451 were significantly declined. 3) In LC-COPD patients, plasma levels of MDA-protein adducts levels were significantly higher, while those of GSH and the expression of miR-210 were significantly declined compared to LC-only patients. 4) In non-CF bronchiectasis patients, plasma MDA-protein adducts, GSH, myeloperoxidase, CRP, ESR, fibrinogen, alpha-1 antitrypsin, IgA, and IgG levels were significantly higher compared to healthy controls. Conclusions: Systemic oxidative and antioxidative markers such as MDA and GSH are differently expressed in LC patients with COPD, thus implying their contributions to the tumor pathogenesis of these patients. Non-CF bronchiectasis, on the other hand, showed an increased level of oxidant and antioxidant markers analyzed. Systemic inflammation takes place in the plasma of LC patients and non-CF bronchiectasis patients; these findings suggest that inflammation may be involved in the pathogenesis of these chronic respiratory diseases. Plasma miRNAs have been shown to be differently expressed in LC patients, specifically miR-451, miR-let 7c, and miR-210; which suggests that those miRNAs may be surrogate markers of lung tumorigenesis that could help monitor patients in the clinics