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The role of ROS/RNS signaling in cardiovascular functions and diseases is increasingly emerging in the last decades. The involvement of ROS/RNS in the control of a large number of cardiovascular functions like the regulation of the vascular tone, the control of blood pressure or myocyte excitation-contraction coupling and force development has been broadly investigated and in part clarified. On the other hand, many efforts have been focused in clarifying the redox mechanisms involved in cardiovascular diseases like ischemia/reperfusion injury, diabetes-associated cardiovascular dysfunctions, atherosclerosis or hypertension, just to mention the major ones. However, in most cases the two levels of investigation remain separate and not interlaced, failing in the attempt to provide a unified vision of the pathophysiologic mechanisms of cardiovascular diseases. The major aim of the Research Topic has been to collect original papers and review articles dealing with the issue from basic to translation research point of views. The topic includes contributions that highlight different interesting aspects of cardiovascular biology with an integrated approach useful for the development of new ideas and advancements in the field of redox signaling in the control of normal cardiovascular functions and their disruption in diseases.
Antioxidants --- Metabolomics --- Stroke --- Exercise --- ischemia/reperfusion injury --- mitochondria and chaperones --- Pulmonary hypertention --- reactive oxygen and nitrogen species --- cardiac preconditioning and postconditioning --- Endothelium
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The role of ROS/RNS signaling in cardiovascular functions and diseases is increasingly emerging in the last decades. The involvement of ROS/RNS in the control of a large number of cardiovascular functions like the regulation of the vascular tone, the control of blood pressure or myocyte excitation-contraction coupling and force development has been broadly investigated and in part clarified. On the other hand, many efforts have been focused in clarifying the redox mechanisms involved in cardiovascular diseases like ischemia/reperfusion injury, diabetes-associated cardiovascular dysfunctions, atherosclerosis or hypertension, just to mention the major ones. However, in most cases the two levels of investigation remain separate and not interlaced, failing in the attempt to provide a unified vision of the pathophysiologic mechanisms of cardiovascular diseases. The major aim of the Research Topic has been to collect original papers and review articles dealing with the issue from basic to translation research point of views. The topic includes contributions that highlight different interesting aspects of cardiovascular biology with an integrated approach useful for the development of new ideas and advancements in the field of redox signaling in the control of normal cardiovascular functions and their disruption in diseases.
Antioxidants --- Metabolomics --- Stroke --- Exercise --- ischemia/reperfusion injury --- mitochondria and chaperones --- Pulmonary hypertention --- reactive oxygen and nitrogen species --- cardiac preconditioning and postconditioning --- Endothelium
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The role of ROS/RNS signaling in cardiovascular functions and diseases is increasingly emerging in the last decades. The involvement of ROS/RNS in the control of a large number of cardiovascular functions like the regulation of the vascular tone, the control of blood pressure or myocyte excitation-contraction coupling and force development has been broadly investigated and in part clarified. On the other hand, many efforts have been focused in clarifying the redox mechanisms involved in cardiovascular diseases like ischemia/reperfusion injury, diabetes-associated cardiovascular dysfunctions, atherosclerosis or hypertension, just to mention the major ones. However, in most cases the two levels of investigation remain separate and not interlaced, failing in the attempt to provide a unified vision of the pathophysiologic mechanisms of cardiovascular diseases. The major aim of the Research Topic has been to collect original papers and review articles dealing with the issue from basic to translation research point of views. The topic includes contributions that highlight different interesting aspects of cardiovascular biology with an integrated approach useful for the development of new ideas and advancements in the field of redox signaling in the control of normal cardiovascular functions and their disruption in diseases.
Antioxidants --- Metabolomics --- Stroke --- Exercise --- ischemia/reperfusion injury --- mitochondria and chaperones --- Pulmonary hypertention --- reactive oxygen and nitrogen species --- cardiac preconditioning and postconditioning --- Endothelium
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Background: Kidney transplantation remains the first-choice treatment for end-stage renal disease (ESRD). The demand for kidney transplants is rising annually and the shortage of organs is becoming more severe. This has led to the criteria for donors being expanded to include donation after circulatory death (DCD) and poorer quality (Senior age, potential medical conditions, etc.) donations after brain death (DBD). They tend to have poorer short- and long-term outcomes. A way needs to be found to mitigate the effects of ischemia-reperfusion injury on the graft in this type of donor. Our previous studies have identified mesenchymal stromal cell (MSC) pre-exposure as a potential treatment, and we hope to further validate its effects in rat DBD and DCD models. Objectif: We aimed to evaluate the effects of MSC pre-exposure on different types of renal grafts through the quantification of kidney injury molecule 1 (KIM-1), a highly sensitive and highly specific biomarker of kidney injury. Methods: Two rat models (DBD and DCD) were established to obtain kidneys in different transplant situations. Two sets of serum samples, one set of urine samples and two kidneys from each rat were obtained during the procedure i: a clinical assessment of renal function (SCr, BUN) was performed. ii: Microarchitecture of grafts assessed by (immuno) histochemistry (PAS staining and KIM-1 IHC). iii: Expression of HAVCR-1 (KIM-1 gene) in tissues was assessed by q-PCR. Conclusions: Our preliminary findings suggest that brain death and cold ischemia exacerbate the extent of kidney injury in rats, and that MSC pre-exposure may have different effects on DCD and DBD. For DBD kidneys, MSC pre-exposure may be a potential means of reducing injury. Further research is required to confirm the results. Background: La transplantation rénale reste le traitement de premier choix de l'insuffisance rénale terminale (IRT). La demande de transplantations rénales augmente chaque année et la pénurie d'organes s'aggrave. Les critères de sélection des donneurs ont donc été élargis pour inclure les dons après la mort circulatoire (DCD) et les dons après la mort cérébrale (DBD) de moins bonne qualité (âge avancé, conditions médicales potentielles, etc.). Ces derniers ont tendance à avoir de moins bons résultats à court et à long terme. Il faut trouver un moyen d'atténuer les effets des lésions d'ischémie-reperfusion sur le greffon chez ce type de donneur. Nos études précédentes ont identifié la pré-exposition aux cellules stromales mésenchymateuses (CSM) comme un traitement potentiel, et nous espérons valider davantage ses effets dans des modèles de DBD et de DCD chez le rat. Objectif: Nous avons voulu évaluer les effets de la pré-exposition des CSM sur différents types de greffons rénaux par la quantification de kidney injury molecule 1 (KIM-1), un biomarqueur très sensible et très spécifique de lésion rénale. Méthodes: Deux modèles de rat (DBD et DCD) ont été établis pour obtenir des reins dans différentes situations de transplantation. Deux séries d'échantillons de sérum, une série d'échantillons d'urine et deux reins de chaque rat ont été prélevés au cours de la procédure : i : une évaluation clinique de la fonction rénale (SCr, BUN) a été réalisée. ii : la microarchitecture des greffons a été évaluée par (immuno) histochimie (coloration PAS et KIM-1 IHC). iii : L'expression du HAVCR-1 (gène KIM-1) dans les tissus a été évaluée par q-PCR. Conclusions: Nos résultats préliminaires suggèrent que la mort cérébrale et l'ischémie froide exacerbent l'étendue des lésions rénales chez les rats, et que la pré-exposition aux CSM peut avoir des effets différents selon le type de doneur. Pour les reins de DBD, la pré-exposition aux CSM peut être un moyen potentiel de réduire les lésions. Des recherches supplémentaires sont nécessaires pour confirmer ces résultats.
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The book “Protective and Detrimental Role of Heme Oxygenase-1”, includes a selection of original research papers and reviews aimed at understanding the dual role (protective and detrimental) of HO-1 and the involved signaling pathways. Original research papers and reviews aimed at the identification of natural molecules or new synthetic compounds able to modulate HO-1 activity/expression help make HO-1 a potential therapeutic target for the amelioration of various diseases.
coronary artery disease --- n/a --- glucocorticoid receptor --- antigen presentation --- analgesia --- chemotherapy --- locus coeruleus --- Sirtuin 1 --- thiol groups --- Heme Oxygenase-1 --- Betula etnensis Raf. --- heme oxygenase 1 --- tolerance --- heme oxygenase --- atherosclerosis --- nitric oxide --- caloric restriction --- liver --- carbon monoxide --- ER stress --- heme oxygenase-1 --- mineralocorticoid receptor --- Type 1 diabetes mellitus (T1D) --- Gamma-Glutamyl-Cysteine Ligase (GGCL) --- angiotensin II --- bilirubin --- Heme oxygenase-1 (HO-1) inducers --- Inducible nitric oxide synthase (iNOS) --- HO-1 activity inhibitor --- ferroptosis --- Myristica fragrans kernels --- glutathione --- high-pressure gas --- apoptosis --- HO-1 --- diabetes mellitus --- Caffeic acid phenethyl ester (CAPE) --- carotid plaque --- ischemia–reperfusion injury --- ANTIGEN presenting cell --- LPS --- endoplasmic reticulum stress --- hemoglobin --- Pancreatic oxidative damage --- Colon cancer --- inflammation --- reactive oxygen species --- inflammatory pain --- paracetamol --- cardiomyopathy --- heme oxigenase-1 --- adipocytes --- sirtuin 1 --- peripheral artery disease --- PGC-1? --- heme --- Reactive oxygen species (ROS) --- metformin --- GR --- prostate cancer --- NF-?B --- hyperbilirubinemia --- iron --- Tet-ON system --- lung preservation --- oxidative stress --- Gunn rats --- Dimethylarginine dimethylaminohydrolase-1 (DDAH-1) --- ischemia-reperfusion injury
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Cerebral ischemia is one of the most common causes of dementia, which develops in more than half of patients after an ischemic episode. The main mechanism is thought to be pathological changes in the hippocampus, especially in the CA1 area, underlying episodic memory impairment, which is the earliest and most important clinical symptom of post-ischemic dementia. The 13 chapters of this book present a new picture of ischemic brain disease, synthesizing the latest data on disease mechanisms, care for patients with this disease, and potential therapeutic targets. The authors present the characteristics of cerebral ischemia from pregnancy and childhood through adolescence to adulthood. The first two chapters provide a snapshot of the anatomy of the cerebral cortex and the hippocampus, the most affected brain structures after cerebral ischemia. This is followed by nine chapters that present a comprehensive view of the pathological mechanisms of cerebral ischemia, and how a deep understanding of these pathomechanisms hold the key for the discovery and development of novel therapies to help patients affected by cerebral ischemia. Chapter 12 shares real-life experience and challenges of rehabilitating patients into the community after cerebral ischemia, and chapter 13 analyzes the social risk variations, including gender inequality, in the reintegration of post-ischemic stroke patients. Although primarily aimed at scientists and clinicians, the contents of the book will be of interest to all those who are interested in cerebral ischemia, including patients and their caregivers.
MJN --- Anatomy of the Cerebral Cortex; Anatomy of the Hippocampus; Genes Associated with Alzheimer’s Disease; Hypoxic-Ischemic Brain Injury; Perinatal Asphyxia; Ischemic Brain Injury; Hyperhomocysteinemia; Exosomes in Post-Ischemic Brain; Neuroinflammation in Post-Ischemic Brain; Neurovascular Reactivity in Cerebral Ischemia; Cathepsin B in Ischemia-Reperfusion Injury After Stroke; Curcumin in Post-Ischemic Brain; Treating Cerebral Ischemia; Experimental Stroke Research; Community-Based Rehabilitation in Japan; Social Risk Variation Across Reintegration of Post-Ischemic Stroke Patients
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Cerebral ischemia is one of the most common causes of dementia, which develops in more than half of patients after an ischemic episode. The main mechanism is thought to be pathological changes in the hippocampus, especially in the CA1 area, underlying episodic memory impairment, which is the earliest and most important clinical symptom of post-ischemic dementia. The 13 chapters of this book present a new picture of ischemic brain disease, synthesizing the latest data on disease mechanisms, care for patients with this disease, and potential therapeutic targets. The authors present the characteristics of cerebral ischemia from pregnancy and childhood through adolescence to adulthood. The first two chapters provide a snapshot of the anatomy of the cerebral cortex and the hippocampus, the most affected brain structures after cerebral ischemia. This is followed by nine chapters that present a comprehensive view of the pathological mechanisms of cerebral ischemia, and how a deep understanding of these pathomechanisms hold the key for the discovery and development of novel therapies to help patients affected by cerebral ischemia. Chapter 12 shares real-life experience and challenges of rehabilitating patients into the community after cerebral ischemia, and chapter 13 analyzes the social risk variations, including gender inequality, in the reintegration of post-ischemic stroke patients. Although primarily aimed at scientists and clinicians, the contents of the book will be of interest to all those who are interested in cerebral ischemia, including patients and their caregivers.
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Cerebral ischemia is one of the most common causes of dementia, which develops in more than half of patients after an ischemic episode. The main mechanism is thought to be pathological changes in the hippocampus, especially in the CA1 area, underlying episodic memory impairment, which is the earliest and most important clinical symptom of post-ischemic dementia. The 13 chapters of this book present a new picture of ischemic brain disease, synthesizing the latest data on disease mechanisms, care for patients with this disease, and potential therapeutic targets. The authors present the characteristics of cerebral ischemia from pregnancy and childhood through adolescence to adulthood. The first two chapters provide a snapshot of the anatomy of the cerebral cortex and the hippocampus, the most affected brain structures after cerebral ischemia. This is followed by nine chapters that present a comprehensive view of the pathological mechanisms of cerebral ischemia, and how a deep understanding of these pathomechanisms hold the key for the discovery and development of novel therapies to help patients affected by cerebral ischemia. Chapter 12 shares real-life experience and challenges of rehabilitating patients into the community after cerebral ischemia, and chapter 13 analyzes the social risk variations, including gender inequality, in the reintegration of post-ischemic stroke patients. Although primarily aimed at scientists and clinicians, the contents of the book will be of interest to all those who are interested in cerebral ischemia, including patients and their caregivers.
MJN --- Anatomy of the Cerebral Cortex; Anatomy of the Hippocampus; Genes Associated with Alzheimer’s Disease; Hypoxic-Ischemic Brain Injury; Perinatal Asphyxia; Ischemic Brain Injury; Hyperhomocysteinemia; Exosomes in Post-Ischemic Brain; Neuroinflammation in Post-Ischemic Brain; Neurovascular Reactivity in Cerebral Ischemia; Cathepsin B in Ischemia-Reperfusion Injury After Stroke; Curcumin in Post-Ischemic Brain; Treating Cerebral Ischemia; Experimental Stroke Research; Community-Based Rehabilitation in Japan; Social Risk Variation Across Reintegration of Post-Ischemic Stroke Patients
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This Special Issue comprises articles related to the effects of genotype and processing conditions on the phenolic compound profile and antioxidant activity of cocoa-derived products, isolation and characterization of antioxidant compounds such as polyphenols and melanoidins from cocoa beans, and assessment of the antioxidant, antioxidative stress and anti-inflammatory effects of cocoa beans and cocoa-derived products. The results of these studies show that it is possible to maintain or increase the biological activity of cocoa beans and their derived products (cocoa powder and chocolate) by choosing appropriate processing conditions and cocoa genotype and origin. The papers published in this Special Issue confirm that cocoa beans and cocoa by-products can be considered as an attractive source material for manufacturing of functional foods and nutraceuticals. This is because they contain many bioactive compounds, mainly polyphenols, including flavonoids (proanthocyaninidins, monomeric flavan-3-ols, and anthocyanins) and phenolic acids, as well as melanoidins. Finally, the in vitro and in vivo studies demonstrate the importance of cocoa antioxidants for the prevention of oxidative stress and inflammation.
Research & information: general --- Biology, life sciences --- Food & society --- cocoa --- chocolate --- polyphenols --- antioxidants --- melanoidins --- theobroma cacao L. --- total phenolic compounds --- antioxidant capacity --- metal-chelating ability --- fourier transform infrared spectroscopy --- flavan-3-ol --- procyanidin --- α-glucosidase --- melanoidin --- Maillard reaction --- (–)-epicatechin --- borderline hypertensive rats --- nitric oxide --- redox balance --- iron --- Nrf2 --- PPAR-γ --- open field --- cocoa by-products --- cherry extract --- oxidative stress --- human endothelial cell --- roasting --- catechin --- epicatechin --- total phenolic content --- Criollo cocoa --- kinetic --- flavonoids --- cocoa extract --- ischemia-reperfusion injury --- apoptosis --- inflammatory markers --- conching --- milk chocolate --- milk powder --- protein --- antioxidant activity --- solid–liquid kinetic extraction --- polyphenol oxidase --- cocoa polyphenols --- heat treatment --- enzyme inactivation --- n/a --- (-)-epicatechin --- solid-liquid kinetic extraction --- Research. --- Biology. --- Food --- Social aspects.
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This Special Issue comprises articles related to the effects of genotype and processing conditions on the phenolic compound profile and antioxidant activity of cocoa-derived products, isolation and characterization of antioxidant compounds such as polyphenols and melanoidins from cocoa beans, and assessment of the antioxidant, antioxidative stress and anti-inflammatory effects of cocoa beans and cocoa-derived products. The results of these studies show that it is possible to maintain or increase the biological activity of cocoa beans and their derived products (cocoa powder and chocolate) by choosing appropriate processing conditions and cocoa genotype and origin. The papers published in this Special Issue confirm that cocoa beans and cocoa by-products can be considered as an attractive source material for manufacturing of functional foods and nutraceuticals. This is because they contain many bioactive compounds, mainly polyphenols, including flavonoids (proanthocyaninidins, monomeric flavan-3-ols, and anthocyanins) and phenolic acids, as well as melanoidins. Finally, the in vitro and in vivo studies demonstrate the importance of cocoa antioxidants for the prevention of oxidative stress and inflammation.
cocoa --- chocolate --- polyphenols --- antioxidants --- melanoidins --- theobroma cacao L. --- total phenolic compounds --- antioxidant capacity --- metal-chelating ability --- fourier transform infrared spectroscopy --- flavan-3-ol --- procyanidin --- α-glucosidase --- melanoidin --- Maillard reaction --- (–)-epicatechin --- borderline hypertensive rats --- nitric oxide --- redox balance --- iron --- Nrf2 --- PPAR-γ --- open field --- cocoa by-products --- cherry extract --- oxidative stress --- human endothelial cell --- roasting --- catechin --- epicatechin --- total phenolic content --- Criollo cocoa --- kinetic --- flavonoids --- cocoa extract --- ischemia-reperfusion injury --- apoptosis --- inflammatory markers --- conching --- milk chocolate --- milk powder --- protein --- antioxidant activity --- solid–liquid kinetic extraction --- polyphenol oxidase --- cocoa polyphenols --- heat treatment --- enzyme inactivation --- n/a --- (-)-epicatechin --- solid-liquid kinetic extraction --- Research. --- Biology. --- Food --- Social aspects.
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