Programmed cell death cellular (22 résultats)

Hardcover. Etat : Très bon. Ancien livre de bibliothèque. Edition 2001. Tome 1. Ammareal reverse jusqu'à 15% du prix net de cet article à des organisations caritatives. ENGLISH DESCRIPTION Book Condition: Used, Very good. Former library book. Edition 2001. Volume 1. Ammareal gives back up to 15% of this item's net price to charity organizations.…

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Hardcover. Etat : Very Good -. None as issued. Clean, solid copy with no writing, highlighting, marks, or creased page corners to text; previous owner's name written on corner of title page. Cover corners and spine ends are bumped. Book has a very slight curve, as if something heavy had been set on it. As a result there are a couple of wrinkles on the front cover. Cover also has light surface scratches front and back. Binding is firm. While the cover shows wear, the pages are like new! We are unable to ship oversize books and multi-volume sets internationally.…

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Buch. Etat : Neu. Neuware - Apoptosis, or programmed cell death, is an adaptive form of cell death that plays a critical role in turnover of mitotic cells and various tissues in the adult, including epithelial cells, fibroblasts and various endocrine cells. Programmed cell death also plays a major role in development in organizing the body plan and molding intricate cellular structures such as nerve cell circuits in the brain. Rapidly progressing research into the molecular and biochemical underpinnings of the programmed cell death process are revealing novel genetic programs and molecular interactions that coordinate a process that results in death and removal of cells without an immune response and in the absence of the adverse effects on neighboring cells. Programmed Cell Death, Volume I, critically details the molecular, biochemical and cellular mechanisms of apoptosis. This volume covers programmed cell death in a variety of tissues and organ systems highlighting the interesting families of proteins involved in promoting or preventing apoptosis. These include the caspase and calpain families of proteases, Bcl-2 family members, and inhibitors of apoptosis proteins. Each chapter is written by an internationally recognized expert in a particular aspect of programmed cell death.This book will provide the reader with a comprehensive understanding of the cascade of events leading from an apoptotic signal, such as trophic factor withdrawal or increased oxidative stress, to cell death. Importantly, this volume also covers signaling mechanisms designed to prevent apoptosis. Such anti-apoptotic signaling cascades involve neurotrophic factors and stress response pathways. Programmed Cell Death, Volume I, provides the molecular and cellular foundation for in which the roles of aberrant regulation of apoptosis in human diseases ranging from cancer to Alzheimer's disease are considered.…

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Hardcover. Etat : Brand New. 1st edition. 350 pages. 10.50x7.25x1.00 inches. In Stock.

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Hardcover. Etat : 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. Etat : 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. Etat : 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.