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Your search keyword '"Martínez‐Moratalla Rovira, Jesús"' showing total 4 results
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4 results on '"Martínez‐Moratalla Rovira, Jesús"'

1. Cross-sectional study on exhaled nitric oxide in relation to upper airway inflammatory disorders with regard to asthma and perennial sensitisation

Author

Krantz, Christina, Accordini, Simone, Alving, Kjell, Corsico, Angelo G, Demoly, Pascal, Ferreira, Diogenes S, Forsberg, Bertil, Garcia-Aymerich, Judith, Gislason, Thorarinn, Heinrich, Joachim, Jõgi, Rain, Johannessen, Ane, Leynaert, Bénédicte, Marcon, Alessandro, Martínez-Moratalla Rovira, Jesús, Nerpin, Elisabet, Nowak, Dennis, Olin, Anna-Carin, Olivieri, Mario, Pereira-Vega, Antonio, Raherison-Semjen, Chantal, Real, Francisco Gómez, Sigsgaard, Torben, Squillacioti, Guilia, Janson, Christer, Malinovschi, Andrei, Krantz, Christina, Accordini, Simone, Alving, Kjell, Corsico, Angelo G, Demoly, Pascal, Ferreira, Diogenes S, Forsberg, Bertil, Garcia-Aymerich, Judith, Gislason, Thorarinn, Heinrich, Joachim, Jõgi, Rain, Johannessen, Ane, Leynaert, Bénédicte, Marcon, Alessandro, Martínez-Moratalla Rovira, Jesús, Nerpin, Elisabet, Nowak, Dennis, Olin, Anna-Carin, Olivieri, Mario, Pereira-Vega, Antonio, Raherison-Semjen, Chantal, Real, Francisco Gómez, Sigsgaard, Torben, Squillacioti, Guilia, Janson, Christer, and Malinovschi, Andrei

Abstract

BACKGROUND: Fractional exhaled nitric oxide (FeNO) is a well-known marker of type-2 inflammation. FeNO is elevated in asthma and allergic rhinitis, with IgE sensitisation as a major determinant. OBJECTIVE: We aimed to see if there was an independent association between upper airway inflammatory disorders (UAID) and FeNO, after adjustment for asthma and sensitisation, in a multi-centre population-based study. METHODS: A total of 741 subjects with current asthma and 4,155 non-asthmatic subjects participating in the second follow-up of the European Community Respiratory Health Survey (ECRHS III) underwent FeNO measurements. Sensitisation status was based on measurement of IgE against airborne allergens; information on asthma, UAID and medication was collected through interview-led questionnaires. Independent associations between UAID and FeNO was assessed in adjusted multivariate regression models and test for interaction with perennial sensitisation and asthma on the relation between UAID and FeNO were made. RESULTS: UAID were associated with higher FeNO after adjusting for perennial sensitisation, asthma and other confounders: with 4.4 (0.9-7.9) % higher FeNO in relation to current rhinitis and 4.8 (0.7-9.2)% higher FeNO in relation to rhinoconjunctivitis. A significant interaction with perennial sensitisation was found in the relationship between current rhinitis and FeNO (p=0.03) and between rhinoconjunctivitis and FeNO (p=0.03). After stratification by asthma and perennial sensitisation, the association between current rhinitis and FeNO remained in non-asthmatic subjects with perennial sensitisation, with 12.1 (0.2-25.5) % higher FeNO in subjects with current rhinitis than in those without. CONCLUSIONS & CLINICAL RELEVANCE: Current rhinitis and rhinoconjunctivitis was associated with higher FeNO, with an interaction with perennial sensitisation. This further highlights the concept of united airway disease, with correlations between symptoms and inflammation in

Published
2022
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2. Prenatal and prepubertal exposures to tobacco smoke in men may cause lower lung function in future offspring: a three-generational study using a causal modelling approach: a three-generation study using a causal modelling approach

Author

Accordini, Simone, Calciano, Lucia, Johannessen, Ane, Benediktsdóttir, Bryndis, Bertelsen, Randi Jacobsen, Bråbäck, Lennart, Dharmage, Shyamali C., Forsberg, Bertil, Real, Francisco Gomez, Holloway, John, Holm, Mathias, Janson, Christer, Jõgi, Nils Oskar, Jögi, Rain, Malinovschi, Andrei, Marcon, Alessandro, Martínez-moratalla Rovira, Jesús, Sánchez-Ramos, José Luis, Schlunssen, Vivi, Torén, Kjell, Jarvis, Deborah, and Svanes, Cecilie

Subjects
respiratory system, circulatory and respiratory physiology, respiratory tract diseases
Abstract

Mechanistic research suggests that lifestyle and environmental factors impact respiratory health across generations by epigenetic changes transmitted through male germ cells. Evidence from studies on humans is very limited.We investigated multigeneration causal associations to estimate the causal effects of tobacco smoking on lung function within the paternal line. We analysed data from 383 adult offspring (age 18-47 years; 52.0% female) and their 274 fathers, who had participated in the European Community Respiratory Health Survey (ECRHS)/Respiratory Health in Northern Europe, Spain and Australia (RHINESSA) generation study and had provided valid measures of pre-bronchodilator lung function. Two counterfactual-based, multilevel mediation models were developed with: paternal grandmothers' smoking in pregnancy and fathers' smoking initiation in prepuberty as exposures; fathers' forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC), or FEV1/FVC z-scores as potential mediators (proxies of unobserved biological mechanisms that are true mediators); and offspring's FEV1 and FVC, or FEV1/FVC z-scores as outcomes. All effects were summarised as differences (Δ) in expected z-scores related to fathers' and grandmothers' smoking history.Fathers' smoking initiation in prepuberty had a negative direct effect on both offspring's FEV1 (Δz-score -0.36, 95% CI -0.63- -0.10) and FVC (-0.50, 95% CI -0.80- -0.20) compared with fathers' never smoking. Paternal grandmothers' smoking in pregnancy had a negative direct effect on fathers' FEV1/FVC (-0.57, 95% CI -1.09- -0.05) and a negative indirect effect on offspring's FEV1/FVC (-0.12, 95% CI -0.21- -0.03) compared with grandmothers' not smoking before fathers' birth nor during fathers' childhood.Fathers' smoking in prepuberty and paternal grandmothers' smoking in pregnancy may cause lower lung function in offspring. Our results support the concept that lifestyle-related exposures during these susceptibility periods influence the health of future generations.

Published
2021

3. Cross-sectional study on exhaled nitric oxide in relation to upper airway inflammatory disorders with regard to asthma and perennial sensitization.

Author

Krantz C, Accordini S, Alving K, Corsico AG, Demoly P, Ferreira DS, Forsberg B, Garcia-Aymerich J, Gislason T, Heinrich J, Jõgi R, Johannessen A, Leynaert B, Marcon A, Martínez-Moratalla Rovira J, Nerpin E, Nowak D, Olin AC, Olivieri M, Pereira-Vega A, Raherison-Semjen C, Real FG, Sigsgaard T, Squillacioti G, Janson C, and Malinovschi A

Subjects
Allergens, Breath Tests, Cross-Sectional Studies, Exhalation, Humans, Asthma complications, Asthma diagnosis, Asthma epidemiology, Nitric Oxide
Abstract

Background: Fractional exhaled nitric oxide (FeNO) is a well-known marker of type-2 inflammation. FeNO is elevated in asthma and allergic rhinitis, with IgE sensitization as a major determinant., Objective: We aimed to see whether there was an independent association between upper airway inflammatory disorders (UAID) and FeNO, after adjustment for asthma and sensitization, in a multi-centre population-based study., Methods: A total of 741 subjects with current asthma and 4155 non-asthmatic subjects participating in the second follow-up of the European Community Respiratory Health Survey (ECRHS III) underwent FeNO measurements. Sensitization status was based on measurement of IgE against airborne allergens; information on asthma, UAID and medication was collected through interview-led questionnaires. Independent associations between UAID and FeNO were assessed in adjusted multivariate regression models and test for interaction with perennial sensitization and asthma on the relation between UAID and FeNO were made., Results: UAID were associated with higher FeNO after adjusting for perennial sensitization, asthma and other confounders: with 4.4 (0.9-7.9) % higher FeNO in relation to current rhinitis and 4.8 (0.7-9.2) % higher FeNO in relation to rhinoconjunctivitis. A significant interaction with perennial sensitization was found in the relationship between current rhinitis and FeNO (p = .03) and between rhinoconjunctivitis and FeNO (p = .03). After stratification by asthma and perennial sensitization, the association between current rhinitis and FeNO remained in non-asthmatic subjects with perennial sensitization, with 12.1 (0.2-25.5) % higher FeNO in subjects with current rhinitis than in those without., Conclusions & Clinical Relevance: Current rhinitis and rhinoconjunctivitis was associated with higher FeNO, with an interaction with perennial sensitization. This further highlights the concept of united airway disease, with correlations between symptoms and inflammation in the upper and lower airways and that sensitization needs to be accounted for in the relation between FeNO and rhinitis., (© 2021 The Authors. Clinical & Experimental Allergy published by John Wiley & Sons Ltd.)

Published
2022
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4. Prenatal and prepubertal exposures to tobacco smoke in men may cause lower lung function in future offspring: a three-generation study using a causal modelling approach.

Author

Accordini S, Calciano L, Johannessen A, Benediktsdóttir B, Bertelsen RJ, Bråbäck L, Dharmage SC, Forsberg B, Gómez Real F, Holloway JW, Holm M, Janson C, Jõgi NO, Jõgi R, Malinovschi A, Marcon A, Martínez-Moratalla Rovira J, Sánchez-Ramos JL, Schlünssen V, Torén K, Jarvis D, and Svanes C

Subjects
Adolescent, Adult, Child, Humans, Middle Aged, Pregnancy, Young Adult, Adult Children, Forced Expiratory Volume, Lung, Nicotiana, Smoking adverse effects, Vital Capacity, Male, Female, Tobacco Smoke Pollution adverse effects
Abstract

Mechanistic research suggests that lifestyle and environmental factors impact respiratory health across generations by epigenetic changes transmitted through male germ cells. Evidence from studies on humans is very limited.We investigated multigeneration causal associations to estimate the causal effects of tobacco smoking on lung function within the paternal line. We analysed data from 383 adult offspring (age 18-47 years; 52.0% female) and their 274 fathers, who had participated in the European Community Respiratory Health Survey (ECRHS)/Respiratory Health in Northern Europe, Spain and Australia (RHINESSA) generation study and had provided valid measures of pre-bronchodilator lung function. Two counterfactual-based, multilevel mediation models were developed with: paternal grandmothers' smoking in pregnancy and fathers' smoking initiation in prepuberty as exposures; fathers' forced expiratory volume in 1 s (FEV 1 ) and forced vital capacity (FVC), or FEV 1 /FVC z-scores as potential mediators (proxies of unobserved biological mechanisms that are true mediators); and offspring's FEV 1 and FVC, or FEV 1 /FVC z-scores as outcomes. All effects were summarised as differences (Δ) in expected z-scores related to fathers' and grandmothers' smoking history.Fathers' smoking initiation in prepuberty had a negative direct effect on both offspring's FEV 1 (Δz-score -0.36, 95% CI -0.63- -0.10) and FVC (-0.50, 95% CI -0.80- -0.20) compared with fathers' never smoking. Paternal grandmothers' smoking in pregnancy had a negative direct effect on fathers' FEV 1 /FVC (-0.57, 95% CI -1.09- -0.05) and a negative indirect effect on offspring's FEV 1 /FVC (-0.12, 95% CI -0.21- -0.03) compared with grandmothers' not smoking before fathers' birth nor during fathers' childhood.Fathers' smoking in prepuberty and paternal grandmothers' smoking in pregnancy may cause lower lung function in offspring. Our results support the concept that lifestyle-related exposures during these susceptibility periods influence the health of future generations., Competing Interests: Conflict of interest: S. Accordini has nothing to disclose. Conflict of interest: L. Calciano has nothing to disclose. Conflict of interest: A. Johannessen has nothing to disclose. Conflict of interest: B. Benediktsdóttir has nothing to disclose. Conflict of interest: R.J. Bertelsen has nothing to disclose. Conflict of interest: L. Bråbäck has nothing to disclose. Conflict of interest: S.C. Dharmage has nothing to disclose. Conflict of interest: B. Forsberg has nothing to disclose. Conflict of interest: F. Gómez Real has nothing to disclose. Conflict of interest: J.W. Holloway reports grants from the European Union's Horizon 2020 research and innovation programme, and from the Research Council of Norway, during the conduct of the study. Conflict of interest: M. Holm has nothing to disclose. Conflict of interest: C. Janson has nothing to disclose. Conflict of interest: N.O. Jõgi has nothing to disclose. Conflict of interest: R. Jõgi reports grants from the Estonian Research Council (personal research grant number 562), during the conduct of the study; personal fees for consultancy and lectures from GSK, Boehringer and Novartis, personal fees for travel/accommodation/meeting expenses from GSK and Boehringer, outside the submitted work. Conflict of interest: A. Malinovschi has nothing to disclose. Conflict of interest: A. Marcon has nothing to disclose. Conflict of interest: J. Martínez-Moratalla Rovira has nothing to disclose. Conflict of interest: J.L. Sánchez-Ramos has nothing to disclose. Conflict of interest: V. Schlünssen has nothing to disclose. Conflict of interest: K. Torén has nothing to disclose. Conflict of interest: D. Jarvis reports grants from the European Union, during the conduct of the study. Conflict of interest: C. Svanes has nothing to disclose., (Copyright ©The authors 2021.)

Published
2021
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