Laura Molinari
Research Subjects
Laura Molinari has a total of 2 co-authors. Here are the top co-authors by number of shared publications:
- Elsa Nervo
Elsa Nervo, Società Chimica Italiana, 00198 Rome, Italy
2 shared publications - Giuliano Molinari
Institute of Electrical and Electronics Engineers
2 shared publications
Latest Publications
- Open Access
- 29 June 2020
- Published by MDPI AG in International Journal of Environmental Research and Public Health
- Vol. 17 (13) , 4688
Environmental and Endogenous Acids Can Trigger Allergic-Type Airway Reactions
Inflammatory allergic and nonallergic respiratory disorders are spreading worldwide and often coexist. The root cause is not clear. This review demonstrates that, from a biochemical point of view, it is ascribable to protons (H+) released into cells by exogenous and endogenous acids. The hypothesis of acids as the common cause stems from two considerations: (a) it has long been known that exogenous acids present in air pollutants can induce the irritation of epithelial surfaces, particularly the airways, inflammation, and bronchospasm; (b) according to recent articles, endogenous acids, generated in cells by phospholipases, play a key role in the biochemical mechanisms of initiation and progression of allergic-type reactions. Therefore, the intracellular acidification and consequent Ca2+ increase, induced by protons generated by either acid pollutants or endogenous phospholipases, may constitute the basic mechanism of the multimorbidity of these disorders, and environmental acidity may contribute to their spread.
- 29 June 2020
- Published by MDPI AG in International Journal of Environmental Research and Public Health
- Vol. 17 (13) , 4688
Open AccessEnvironmental and Endogenous Acids Can Trigger Allergic-Type Airway Reactions
Inflammatory allergic and nonallergic respiratory disorders are spreading worldwide and often coexist. The root cause is not clear. This review demonstrates that, from a biochemical point of view, it is ascribable to protons (H+) released into cells by exogenous and endogenous acids. The hypothesis of acids as the common cause stems from two considerations: (a) it has long been known that exogenous acids present in air pollutants can induce the irritation of epithelial surfaces, particularly the airways, inflammation, and bronchospasm; (b) according to recent articles, endogenous acids, generated in cells by phospholipases, play a key role in the biochemical mechanisms of initiation and progression of allergic-type reactions. Therefore, the intracellular acidification and consequent Ca2+ increase, induced by protons generated by either acid pollutants or endogenous phospholipases, may constitute the basic mechanism of the multimorbidity of these disorders, and environmental acidity may contribute to their spread.
- Open Access
- 5 June 2019
- Published by MDPI AG in Preprints.org
Acids Can Promote the Onset and Multimorbidity of Allergic and Nonallergic Airway Diseases
Inflammatory allergic and nonallergic respiratory pathologies often co-exist . The root cause is not clear. This paper demonstrates that it is ascribable to protons (H+) released into cells by exogenous and endogenous acids. The hypothesis of acids as the common cause stems from two considerations: a) it has long been known that exogenous acids present in air pollutants can induce the irritation of epithelial surfaces, particularly the airways, inflammation and bronchospasm; b) according to recent articles, endogenous acids, generated in cells by phospholipases, play a key role in the biochemical mechanisms of initiation and progression of allergic responses. Therefore, the intracellular acidification and consequent Ca2+ increase, induced by protons generated by either acid pollutants or endogenous phospholipases, may be the causal mechanism of the multimorbidity of these diseases, and environmental acidity may contribute to their spread.
- 5 June 2019
- Published by MDPI AG in Preprints.org
Open AccessAcids Can Promote the Onset and Multimorbidity of Allergic and Nonallergic Airway Diseases
Inflammatory allergic and nonallergic respiratory pathologies often co-exist . The root cause is not clear. This paper demonstrates that it is ascribable to protons (H+) released into cells by exogenous and endogenous acids. The hypothesis of acids as the common cause stems from two considerations: a) it has long been known that exogenous acids present in air pollutants can induce the irritation of epithelial surfaces, particularly the airways, inflammation and bronchospasm; b) according to recent articles, endogenous acids, generated in cells by phospholipases, play a key role in the biochemical mechanisms of initiation and progression of allergic responses. Therefore, the intracellular acidification and consequent Ca2+ increase, induced by protons generated by either acid pollutants or endogenous phospholipases, may be the causal mechanism of the multimorbidity of these diseases, and environmental acidity may contribute to their spread.