Isbn: 9783725865307 - cellular redox mechanisms in inflammation and programmed cell death (9 Ergebnisse)

HRD. Zustand: New. New Book. Shipped from UK. Established seller since 2000.

HRD. Zustand: New. New Book. Shipped from UK. Established seller since 2000.

Zustand: New.

Zustand: New. Print on Demand.

Zustand: New. Print on Demand.

Zustand: New. PRINT ON DEMAND.

Hardcover. Zustand: new. Hardcover. Redox reactions play an important role in the regulation of various physiological processes, resulting in the diversity of articles featured in this Special Issue (SI), from works studying mechanisms of antioxidant activity to a prospective randomized study of the effects of hypoxia-hyperoxia exposures on metabolic products of the intestinal microbiome in patients. In vitro, microbiota metabolites formed under inflammation and sepsis inhibit cyclooxygenase peroxidase activity. Macrophages are the most persistent cells at inflammatory sites, with phenotypes differing not only in cytokine secretion but also in the production of reactive oxygen species (ROS). Neuronal dysfunction and pain may be caused by an imbalance in ROS/reactive nitrogen species (RNS) and antioxidant defense; thus, compounds with antioxidant properties can be promising therapeutic agents to mitigate oxidative stress and alleviate pathological conditions. An example of this is manganese porphyrins, which target key pathways involved in neuropathic pain. In this SI, flavonoids, polyphenols, and selenium compounds are studied for their protective ability against inflammation and oxidative injury. Pre-treatment with ferroptosis inhibitors or maintenance of mitochondrial functions enables the safe rewarming of cooled cells. In contrast, excess glutamate triggers a cascade of oxidative and metabolic disorders causing neuronal ferroptosis, with mitochondria playing a central role in this vulnerability. While diverse in biological models, the articles in this SI all demonstrate that ROS/RNS disorder is both a driver of pathology and a target for therapeutic intervention. This item is printed on demand. Shipping may be from our UK warehouse or from our Australian or US warehouses, depending on stock availability.…

Buch. Zustand: Neu. nach der Bestellung gedruckt Neuware - Printed after ordering - Redox reactions play an important role in the regulation of various physiological processes, resulting in the diversity of articles featured in this Special Issue (SI), from works studying mechanisms of antioxidant activity to a prospective randomized study of the effects of hypoxia-hyperoxia exposures on metabolic products of the intestinal microbiome in patients. In vitro, microbiota metabolites formed under inflammation and sepsis inhibit cyclooxygenase peroxidase activity. Macrophages are the most persistent cells at inflammatory sites, with phenotypes differing not only in cytokine secretion but also in the production of reactive oxygen species (ROS). Neuronal dysfunction and pain may be caused by an imbalance in ROS/reactive nitrogen species (RNS) and antioxidant defense; thus, compounds with antioxidant properties can be promising therapeutic agents to mitigate oxidative stress and alleviate pathological conditions. An example of this is manganese porphyrins, which target key pathways involved in neuropathic pain. In this SI, flavonoids, polyphenols, and selenium compounds are studied for their protective ability against inflammation and oxidative injury. Pre-treatment with ferroptosis inhibitors or maintenance of mitochondrial functions enables the safe rewarming of cooled cells. In contrast, excess glutamate triggers a cascade of oxidative and metabolic disorders causing neuronal ferroptosis, with mitochondria playing a central role in this vulnerability. While diverse in biological models, the articles in this SI all demonstrate that ROS/RNS disorder is both a driver of pathology and a target for therapeutic intervention.…

Buch. Zustand: Neu. Cellular Redox Mechanisms in Inflammation and Programmed Cell Death | Buch | Englisch | 2026 | MDPI AG | EAN 9783725865307 | Verantwortliche Person für die EU: Libri GmbH, Europaallee 1, 36244 Bad Hersfeld, gpsr[at]libri[dot]de | Anbieter: preigu Print on Demand.