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Endocrine and immune parameters, namely glucocorticoid receptors (GcR) and IFN-gamma production in peripheral blood mononuclear cells (PBMC), and corticosterone in plasma, were studied in groups of four male rabbits observed in seminatural conditions in relation to agonistic behaviour and to seasonal variations. These parameters were selected on the basis of the findings that the presence of GcR in PBMC gives an indication of the in vivo biological effects of glucocorticoids and that PBMC cytokine production and plasma corticosterone are related to social behaviour. The frequency of active and passive behaviours was used to rank the animals. Seasonal variations were present for agonistic behaviours (Attack, Follow, Chase) and For plasma corticosterone, which were significantly higher in winter. IFN-gamma production in PBMC was increased after social interactions in both seasons, while plasma corticosterone was increased only in winter: GcR capacity in PBMC was decreased after social interactions. The results indicate that social and physical environmental factors are correlated with immune-endocrine functions

Agonistic behaviour,seasonal variation,corticosterone,glucocorticoid receptors,ifn-gamma production,rabbit. --- Agonistic behaviour. --- Agonistic. --- Animal. --- Animals. --- Behavior. --- Behaviour. --- Blood mononuclear-cells. --- Blood. --- Corticosterone. --- Dominance. --- Endocrine. --- Frequency. --- Function. --- Glucocorticoid receptors. --- Glucocorticoid. --- Glucocorticoids. --- Group. --- Hippocampal electrical-activity. --- Immune. --- Interaction. --- Interactions. --- Invivo. --- Male. --- Parameters. --- Physical. --- Pituitary. --- Plasma corticosterone. --- Plasma-corticosterone. --- Plasma. --- Production. --- Rabbit. --- Rabbits. --- Rank. --- Receptor. --- Receptors. --- Release. --- Responses. --- Season. --- Seasonal variation. --- Social behaviour. --- Social interaction. --- Social interactions. --- Social-interaction. --- Social. --- Stress. --- Variation.

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We have entered a new era where some concepts of the complex community of microorganisms (microbiota comprising bacteria, fungi, viruses, bacteriophages and helminths) are being re-discovered and re-visited. Microbiota and human interaction is not new; they have shared a long history of co-existence. Nevertheless, the opportunities to understand the role of these microorganisms in human diseases and to design a potential treatment were limited. At present, thanks to development of innovative and cutting-edge molecular biological and microbiological technologies as well as clinical informatics and bioinformatics skills, microbiome application is moving into clinics. Approaches to therapy based on prebiotics, probiotics and lately on fecal microbiota transplantation has revolutionized medicine. Microbiota outnumbers our genes and is now regarded as another organ of the body. The gastrointestinal tract and gut microbiota display a well-documented symbiotic relationship. Disruption of intestinal microbiota homeostasis—called dysbiosis—has been associated with several diseases. Whether dysbiosis is a cause or consequence of disease initiation and progression still needs to be investigated in more depth. The aim of this book is to highlight recent advances in the field of microbiome research, which are now shaping medicine, and current approaches to microbiome-oriented therapy for gastrointestinal diseases. Dr. Rinaldo Pellicano Dr. Sharmila Fagoonee Guest Editors

Public health & preventive medicine --- Bacteroides ovatus --- Bifidobacterium adolescentis --- Dysbiosis --- Faecalibacterium prausnitzii --- Ruminococcus gnavus --- type 1 diabetes --- microbiota --- microbiome --- auto-immunity --- gut permeability --- gut --- IBS --- celiac disease --- enteropathy --- gluten --- therapy --- gut microbiota --- precision medicine --- Clostridium difficile --- inflammatory bowel disease --- ulcerative colitis --- irritable bowel disease --- metabolic syndrome --- gastric microbiota --- transient --- persistent --- culture --- sequencing --- Helicobacter pylori --- fecal microbiota transplantation --- feces donor --- fecal microbiota --- flow cytometry --- viability of bacteria --- next-generation sequencing --- culturing of fecal microbiota --- Alzheimer’s disease --- microbiota–gut–brain axis --- neurodegenerative disease --- intestinal flora --- necrotizing enterocolitis --- intestinal microbiology --- infant gut --- metabolomics --- IL-6 --- IL-8 --- IL-12p70 --- intestinal permeability --- zonulin --- gut virome --- steatosis --- cirrhosis --- hepatocellular carcinoma --- gastrointestinal --- technology --- high-throughput --- crohn’s disease --- mononuclear cells --- transient receptor potential channel --- pancreatic diseases --- acute pancreatitis --- chronic pancreatitis --- diabetes mellitus --- pancreatic ductal adenocarcinoma --- pancreatic cystic neoplasms

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The postprandial period is the metabolic phase that directly follows the ingestion of a meal. This period is critical to the handling of nutrients to feed the body throughout the whole day but it is also a time of challenge for the body’s metabolism, which has to be flexible and adaptable regarding the quantity and the quality of the nutrient intake. Changes in postprandial metabolism have been considered to be potential early markers in the pathophysiological course, finally leading to an increased risk of disease development. This book aimed to broaden and add to the research on the importance of postprandial metabolism in nutrition. The book includes literature reviews that cover the broad state of the art of our knowledge about postprandial metabolism, fine original studies of the complex changes in metabolism, and the physiological processes that are considered to drive the onset of pathogenesis. Finally, a series of examples on how nutrient content (especially proteins, sucrose, and lipids) can influence the postprandial metabolism over a wide range of phenomena operating during the postprandial period and how they could contribute to tipping the body towards adverse health processes.

peripheral blood mononuclear cells --- postprandial metabolism --- high fat–high sugar diet --- minipig --- adipose tissue --- biomarkers --- glucose --- human --- night --- postprandial --- wheat albumin --- energy expenditure --- fat oxidation --- respiratory quotient --- sucrose overfeeding --- hepatic steatosis --- intramyocellular lipids --- intrahepatocellular lipids --- dietary protein content --- dietary fat content --- plasma triglyceride --- liver --- gut --- obesity --- amino acid --- lactate --- nutrient flux --- short chain fatty acid --- aging --- catabolic state --- anabolic resistance --- protein synthesis --- energy bolus --- postprandial lipemia --- coconut oil --- butter --- canola oil --- olive oil --- lipid --- triglycerides --- dietary fat --- saturated fat --- cardiovascular disease --- carbohydrates --- cholesterol --- fibers --- food structure --- lipids --- polyphenols --- proteins --- vitamins --- ADMA --- arginine --- SDMA --- DMA --- PRMT --- alpha-glucosidase inhibitor --- biopeptides --- blood glucose --- glycemic control --- hyperglycemia --- milk peptides --- prediabetes --- pre-meal --- type 2 diabetes --- metabolic syndrome --- endothelial function --- oxidative stress --- nuts --- berries --- LBP --- sCD14 --- postprandial kinetics --- high-fat diet

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Dear Colleagues, The brain is vulnerable to injury. Following injury in the brain, apoptosis or necrosis may occur easily, leading to various functional disabilities. Neuronal death is associated with a number of neurological disorders including hypoxic ischemia, epileptic seizures, and neurodegenerative diseases. The brain subjected to injury is regarded to be responsible for the alterations in neurotransmission processes, resulting in functional changes. Oxidative stress produced by reactive oxygen species has been shown to be related to the death of neurons in traumatic injury, stroke, and neurodegenerative diseases. Therefore, scavenging or decreasing free radicals may be crucial for preventing neural tissues from harmful adversities in the brain. Neurotrophic factors, bioactive compounds, dietary nutrients, or cell engineering may ameliorate the pathological processes related to neuronal death or neurodegeneration and appear beneficial for improving neuroprotection. As a result of neuronal death or neuroprotection, the brain undergoes activity-dependent long-lasting changes in synaptic transmission, which is also known as functional plasticity. Neuroprotection implying the rescue from neuronal death is now becoming one of global health concerns. This Special Issue attempts to explore the recent advances in neuroprotection related to the brain. This Special Issue welcomes original research or review papers demonstrating the mechanisms of neuroprotection against brain injury using in vivo or in vitro models of animals as well as in clinical settings. The issues in a paper should be supported by sufficient data or evidence. Prof. Bae Hwan Lee Guest Editor

Research & information: general --- global cerebral ischemia --- amiloride --- sodium-hydrogen exchanger-1 --- zinc --- neuronal death --- neuroprotection --- neurodegenerative disorder --- choline acetyltransferase (ChAT) --- trimethyltin (TMT) --- bean phosphatidylserine (Bean-PS) --- brain-derived neurotrophic factor --- moderate hypoxia --- physical exercise --- psychomotor function --- reaction time --- cortisol --- catecholamines --- nitrite --- endotheline-1 --- lactate --- pyridoxine deficiency --- ischemia --- gerbil --- homocysteine --- cell death --- glia --- neurogenesis --- N-acetyl-l-cysteine --- transient receptor potential melastatin 2 --- neurodegeneration --- Alzheimer's disease --- metabolic disease --- adiponectin --- insulin --- antioxidants --- stroke --- preventive gene therapy --- adenoviral vector --- VEGF --- GDNF --- NCAM --- human umbilical cord blood mononuclear cells --- antioxidant --- brain --- neurodegenerative disease --- oxidative stress --- PGC-1α --- vascular endothelial growth factor --- vascular endothelial growth factor receptor 2 --- PI3K/AKT --- MEK/ERK --- status epilepticus --- hippocampus --- middle cerebral artery occlusion --- reperfusion injury --- lipid emulsion --- excitotoxicity --- apoptosis --- GPR4 receptor --- MPP+ --- Parkinson's disease --- CRISPR/cas9 --- ischemic stroke --- blood brain barrier --- nanoparticle-based drug delivery --- brain targeting --- BDNF --- miRNAs --- synaptic plasticity --- depression --- glioblastoma --- astrocytes --- astrocytic networks --- connexin 43 --- calcium activity --- neural injury --- nimodipine --- subarachnoid haemorrhage --- acid-sensing ion channels --- oxygen-glucose deprivation --- liver growth factor --- inflammation --- microglia --- Tg2576 transgenic mice --- amyloid-beta --- oculomotor system --- trophic factors --- motoneurons --- axotomy --- amyotrophic lateral sclerosis --- electroneutral transport --- cation-chloride cotransporters --- KCCs --- NKCCs --- WNK-SPAK/OSR1 --- ascorbic acid --- aging --- organotypic hippocampal slice culture --- global cerebral ischemia --- amiloride --- sodium-hydrogen exchanger-1 --- zinc --- neuronal death --- neuroprotection --- neurodegenerative disorder --- choline acetyltransferase (ChAT) --- trimethyltin (TMT) --- bean phosphatidylserine (Bean-PS) --- brain-derived neurotrophic factor --- moderate hypoxia --- physical exercise --- psychomotor function --- reaction time --- cortisol --- catecholamines --- nitrite --- endotheline-1 --- lactate --- pyridoxine deficiency --- ischemia --- gerbil --- homocysteine --- cell death --- glia --- neurogenesis --- N-acetyl-l-cysteine --- transient receptor potential melastatin 2 --- neurodegeneration --- Alzheimer's disease --- metabolic disease --- adiponectin --- insulin --- antioxidants --- stroke --- preventive gene therapy --- adenoviral vector --- VEGF --- GDNF --- NCAM --- human umbilical cord blood mononuclear cells --- antioxidant --- brain --- neurodegenerative disease --- oxidative stress --- PGC-1α --- vascular endothelial growth factor --- vascular endothelial growth factor receptor 2 --- PI3K/AKT --- MEK/ERK --- status epilepticus --- hippocampus --- middle cerebral artery occlusion --- reperfusion injury --- lipid emulsion --- excitotoxicity --- apoptosis --- GPR4 receptor --- MPP+ --- Parkinson's disease --- CRISPR/cas9 --- ischemic stroke --- blood brain barrier --- nanoparticle-based drug delivery --- brain targeting --- BDNF --- miRNAs --- synaptic plasticity --- depression --- glioblastoma --- astrocytes --- astrocytic networks --- connexin 43 --- calcium activity --- neural injury --- nimodipine --- subarachnoid haemorrhage --- acid-sensing ion channels --- oxygen-glucose deprivation --- liver growth factor --- inflammation --- microglia --- Tg2576 transgenic mice --- amyloid-beta --- oculomotor system --- trophic factors --- motoneurons --- axotomy --- amyotrophic lateral sclerosis --- electroneutral transport --- cation-chloride cotransporters --- KCCs --- NKCCs --- WNK-SPAK/OSR1 --- ascorbic acid --- aging --- organotypic hippocampal slice culture

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Dear Colleagues, The brain is vulnerable to injury. Following injury in the brain, apoptosis or necrosis may occur easily, leading to various functional disabilities. Neuronal death is associated with a number of neurological disorders including hypoxic ischemia, epileptic seizures, and neurodegenerative diseases. The brain subjected to injury is regarded to be responsible for the alterations in neurotransmission processes, resulting in functional changes. Oxidative stress produced by reactive oxygen species has been shown to be related to the death of neurons in traumatic injury, stroke, and neurodegenerative diseases. Therefore, scavenging or decreasing free radicals may be crucial for preventing neural tissues from harmful adversities in the brain. Neurotrophic factors, bioactive compounds, dietary nutrients, or cell engineering may ameliorate the pathological processes related to neuronal death or neurodegeneration and appear beneficial for improving neuroprotection. As a result of neuronal death or neuroprotection, the brain undergoes activity-dependent long-lasting changes in synaptic transmission, which is also known as functional plasticity. Neuroprotection implying the rescue from neuronal death is now becoming one of global health concerns. This Special Issue attempts to explore the recent advances in neuroprotection related to the brain. This Special Issue welcomes original research or review papers demonstrating the mechanisms of neuroprotection against brain injury using in vivo or in vitro models of animals as well as in clinical settings. The issues in a paper should be supported by sufficient data or evidence. Prof. Bae Hwan Lee Guest Editor

global cerebral ischemia --- amiloride --- sodium–hydrogen exchanger-1 --- zinc --- neuronal death --- neuroprotection --- neurodegenerative disorder --- choline acetyltransferase (ChAT) --- trimethyltin (TMT) --- bean phosphatidylserine (Bean-PS) --- brain-derived neurotrophic factor --- moderate hypoxia --- physical exercise --- psychomotor function --- reaction time --- cortisol --- catecholamines --- nitrite --- endotheline-1 --- lactate --- pyridoxine deficiency --- ischemia --- gerbil --- homocysteine --- cell death --- glia --- neurogenesis --- N-acetyl-l-cysteine --- transient receptor potential melastatin 2 --- neurodegeneration --- Alzheimer’s disease --- metabolic disease --- adiponectin --- insulin --- antioxidants --- stroke --- preventive gene therapy --- adenoviral vector --- VEGF --- GDNF --- NCAM --- human umbilical cord blood mononuclear cells --- antioxidant --- brain --- neurodegenerative disease --- oxidative stress --- PGC-1α --- vascular endothelial growth factor --- vascular endothelial growth factor receptor 2 --- PI3K/AKT --- MEK/ERK --- status epilepticus --- hippocampus --- middle cerebral artery occlusion --- reperfusion injury --- lipid emulsion --- excitotoxicity --- apoptosis --- GPR4 receptor --- MPP+ --- Parkinson’s disease --- CRISPR/cas9 --- ischemic stroke --- blood brain barrier --- nanoparticle-based drug delivery --- brain targeting --- BDNF --- miRNAs --- synaptic plasticity --- depression --- glioblastoma --- astrocytes --- astrocytic networks --- connexin 43 --- calcium activity --- neural injury --- nimodipine --- subarachnoid haemorrhage --- acid-sensing ion channels --- oxygen-glucose deprivation --- liver growth factor --- inflammation --- microglia --- Tg2576 transgenic mice --- amyloid-beta --- oculomotor system --- trophic factors --- motoneurons --- axotomy --- amyotrophic lateral sclerosis --- electroneutral transport --- cation-chloride cotransporters --- KCCs --- NKCCs --- WNK-SPAK/OSR1 --- ascorbic acid --- aging --- organotypic hippocampal slice culture --- n/a --- sodium-hydrogen exchanger-1 --- Alzheimer's disease --- Parkinson's disease