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Staphylococcus aureus is a common inhabitant of the human body with which we co-exist. However, this species can also cause disease in humans when an appropriate opportunity arises, such as a cut or some other breakdown in our body’s defenses. S. aureus is able to initiate infections due, in part, to the diverse group of toxins that they secrete. The exotoxins produced by S. aureus can cause direct damage, thwart our own body’s defenses, or trigger massive amounts of cytokines that lead to indirect damage within the human body. In this book are 12 research articles that deal with different aspects of staphylococcal exotoxins. Some of the work gives an overview about how the toxins contribute to the disease process. Other articles discuss different aspects of several exotoxins, and two articles are centered on countermeasures against S. aureus infections. Overall, this book will give the reader a good overview of how staphylococcal exotoxins contribute to initiating and sustaining infections in humans.

n/a --- HigBA --- cell physiology --- airway epithelial cells --- PPIase --- atopic dermatitis --- adaptive immunity --- staphylococcal enterotoxin --- sortase A --- canned meat --- inhibitor --- innate immunity --- low cytotoxic strains --- Staphylococcus aureus --- in vivo models --- toxin neutralization --- enterotoxin --- LukGH --- PSMs --- microbiome --- eye --- molecular mechanism --- chronic infection --- gene regulation --- toxins --- alpha-toxin --- superantigen-like protein --- fermentation --- erianin --- PpiB --- HACCP --- infection --- enzymes --- methicillin-resistant Staphylococcus aureus --- virulence factor --- enterotoxins --- mouse abscess --- toxin-antitoxin systems --- S. aureus --- polyclonal antibody --- defined minimal medium --- mastitis --- butyric acid derivative --- LukAB --- toxoid vaccine --- superantigen --- pathogenicity islands --- PrsA --- sphingomyelin --- Leukocidin --- lux fusion

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ROS were long considered one of the key players in tissue injury. Indeed, overproduction of ROS results in oxidative stress, a process leading to the development of many pathological conditions. For the treatment of these conditions, the use of antioxidants was proposed. Over time, it was shown that ROS at low concentrations act as signaling molecules, leading to the regulation of physiological functions. Moreover, several interventions that increase ROS generation activate stress-adaptive responses that extend the lifespan. It was also shown that excessive use of antioxidants can counter the beneficial effects of ROS. Currently, much progress has been made in understanding the role of ROS in human diseases and aging, as well as in the regulation of physiological functions, and in identifying the signaling pathways involved in ROS. However, much remains to be understood about the mutual interactions among signaling pathways underlying organisms’ adaptive responses, their modifications (which occur during aging), and some disease states. The aim of this Special Issue is to underline the effects of ROS production and antioxidant treatment in living organisms, focusing on their impact on health, disease, and aging.

CTCL --- apoptosis --- cell viability --- c-FLIP --- XIAP --- artemisinin --- SH-SY5Y cells --- hippocampal neurons --- H2O2 --- AMPK pathway --- atherosclerosis --- sphingomyelin synthase 2 --- endothelial dysfunction --- endoplasmic reticulum stress --- β-catenin --- insulin resistance --- cancer --- cardiovascular disease --- neurodegenerative disorders --- exercise --- mitochondria --- oxidative stress --- PGC-1 --- Nrf2 --- UCPs --- ROS --- light --- DNA damage --- evolution --- D-box --- cavefish --- Spalax --- trimethylamine N-oxide --- cardiomyocytes --- cardiotoxicity --- mitochondrial membrane potential --- CORM-2 --- NADPH oxidase --- AP-1 --- HO-1 --- Renal cell carcinoma (RCC) --- reactive oxygen species (ROS) --- glutathione (GSH) metabolism --- cancer therapy --- clear cell RCC --- papillary RCC --- chromophobe RCC --- sarcopenia --- reactive oxygen species --- redox signaling --- antioxidant supplementation --- protein aggregation --- redox --- proteinopathy --- peroxiredoxins --- tumorigenesis --- ROS scavengers --- n/a

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Phospholipases are a ubiquitous group of enzymes that hydrolyze ester bonds within membrane phospholipids. These enzymes serve multiple biological functions that go far beyond a mere membrane remodeling role in cellular homeostasis; they also play key functions in nutrient digestion and the regulated formation of bioactive lipids involved in cell signaling. It is to the latter function, critical to life, that this book is primarily concerned with. All the chapters are written by renowned experts in the area, and provide forefront information on the role phospholipases in a number of physiological and pathophysiological settings.

inhibitor --- metabolic stability --- α-methylation --- oxoesters --- phospholipase A2 --- adrenic acid --- arachidonic acid --- mass spectrometry --- lipid signaling --- inflammation --- monocytes/macrophages --- crotoxin --- snake venom --- lung impairment --- inflammatory response --- lipid mediators --- neuromuscular blocker --- lipidomics --- PAP-2 --- autotaxin --- lysophosphatidate --- G protein-coupled receptor --- PLA2G6 --- fatty liver --- phospholipid remodeling --- diet-induced obesity --- morbidly obesity --- choline and methionine deficiency --- glioblastoma --- sphingolipid --- sphingosine-1-phosphate --- sphingomyelinase --- sphingomyelin --- metastasis --- phosphatidic acid --- diacylglycerol --- lipin --- signaling --- cPLA2α --- psoriasis --- proliferation --- anti-inflammatory --- atherosclerosis --- phospholipases --- macrophages --- T cells --- lipins --- pancreatic islets --- β-cells --- insulin secretion --- glucose tolerance --- insulin resistance --- group VIA phospholipase A2 --- fatty acid --- knockout mouse --- lipid mediator --- lysophospholipid --- membrane --- phospholipid --- ceramide --- acidic sphingomyelinase --- neutral sphingomyelinase --- hepatocellular carcinoma --- alcoholic and nonalcoholic steatohepatitis --- preadipocytes --- prostaglandins --- adipokines --- cytokines --- EP receptors --- Group V phospholipase A2 --- lipids --- majeed syndrome --- LPIN2 --- LIPIN2 --- chronic non-bacterial osteomyelitis --- chronic recurrent multifocal osteomyelitis --- autoinflammatory --- inflammasome --- macrophage --- osteoclast --- n/a

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Even though initially considered as a passive means for storing energy, lipids are now regarded as multifaceted molecules with crucial structural and functional activities. For instance, some of them play essential roles as key components of cell membranes whereas others act as signaling molecules in the regulation of cell homeostasis. In recent years, lipid research has attracted increasing interest because of the involvement of this class of compounds in human health. Indeed, a plethora of pathological conditions are characterized by alterations in lipid metabolism, such as cardiovascular diseases and brain disorders. This Special Issue is a collection of papers from different experts in lipid research, with the aim of providing new insights into the physiopathological involvement of lipids and their impact on human health. This collection also demonstrates the usefulness of interdisciplinary approaches in the development of novel methods to study and manipulate lipid metabolism, which may represent an attractive target for designing effective therapeutic strategies to counteract numerous pathologies.

Medicine --- neutral sphingomyelinase --- radiation --- sphingomyelin metabolism --- pathology --- cell signaling --- brain --- adipose tissue --- breast cancer --- epinephrine --- breast reconstruction --- epicardial fat thickness --- visceral fat thickness --- high-sensitivity c-reactive protein --- leptin --- gender --- female --- hippocampus --- frontal cortex --- adiponectin --- haptoglobin --- lipocalin --- BDNF --- synaptic proteins --- phosphatidylinositol 4,5-bisphosphate --- phospholipase C --- cholesterol --- high-cholesterol diet --- BET proteins --- cell proliferation --- epigenetics --- HMGCR --- JQ1 --- LDLr --- lipid metabolism --- SREBP --- TMEM97 --- atherosclerosis --- diabetes mellitus --- cardiovascular disease --- chronic inflammation --- hyperglycemia --- mutations --- lipid --- fatty acid --- glyceride --- steroid --- phospholipid --- oral drug absorption --- prodrug --- phospholipase A2 (PLA2) --- acid sphingomyelinase --- SOD --- liver --- eicosanoids --- ischemic stroke --- ischemia --- lipoproteins --- polyunsaturated fatty acids --- angiogenesis --- high-density lipoprotein --- endothelial cell --- metabolism --- metabolic reprogramming --- pulmonary fibrosis --- lipid mediators --- sphingolipids --- sphingosine-1-phosphate --- sphingosine kinase 1 --- prostaglandins --- lysophosphatidic acid --- autotaxin --- G-protein coupled receptors --- lysocardiolipin acyltransferase --- phospholipase D --- oxidized phospholipids --- DNA damage response --- double strand breaks --- ATM --- ionizing radiation --- metabolic stress --- oxidative stress --- p53 --- nuclear sphingolipids --- lipophagy --- lipolysis --- lipid droplets --- lipid storage diseases --- lipid metabolism diseases --- mTORC1 --- TFEB --- Cholesterol --- Fatty acids --- Lipid mediators --- Lipids --- Lipophagy --- Sphingolipids --- neutral sphingomyelinase --- radiation --- sphingomyelin metabolism --- pathology --- cell signaling --- brain --- adipose tissue --- breast cancer --- epinephrine --- breast reconstruction --- epicardial fat thickness --- visceral fat thickness --- high-sensitivity c-reactive protein --- leptin --- gender --- female --- hippocampus --- frontal cortex --- adiponectin --- haptoglobin --- lipocalin --- BDNF --- synaptic proteins --- phosphatidylinositol 4,5-bisphosphate --- phospholipase C --- cholesterol --- high-cholesterol diet --- BET proteins --- cell proliferation --- epigenetics --- HMGCR --- JQ1 --- LDLr --- lipid metabolism --- SREBP --- TMEM97 --- atherosclerosis --- diabetes mellitus --- cardiovascular disease --- chronic inflammation --- hyperglycemia --- mutations --- lipid --- fatty acid --- glyceride --- steroid --- phospholipid --- oral drug absorption --- prodrug --- phospholipase A2 (PLA2) --- acid sphingomyelinase --- SOD --- liver --- eicosanoids --- ischemic stroke --- ischemia --- lipoproteins --- polyunsaturated fatty acids --- angiogenesis --- high-density lipoprotein --- endothelial cell --- metabolism --- metabolic reprogramming --- pulmonary fibrosis --- lipid mediators --- sphingolipids --- sphingosine-1-phosphate --- sphingosine kinase 1 --- prostaglandins --- lysophosphatidic acid --- autotaxin --- G-protein coupled receptors --- lysocardiolipin acyltransferase --- phospholipase D --- oxidized phospholipids --- DNA damage response --- double strand breaks --- ATM --- ionizing radiation --- metabolic stress --- oxidative stress --- p53 --- nuclear sphingolipids --- lipophagy --- lipolysis --- lipid droplets --- lipid storage diseases --- lipid metabolism diseases --- mTORC1 --- TFEB --- Cholesterol --- Fatty acids --- Lipid mediators --- Lipids --- Lipophagy --- Sphingolipids

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Even though initially considered as a passive means for storing energy, lipids are now regarded as multifaceted molecules with crucial structural and functional activities. For instance, some of them play essential roles as key components of cell membranes whereas others act as signaling molecules in the regulation of cell homeostasis. In recent years, lipid research has attracted increasing interest because of the involvement of this class of compounds in human health. Indeed, a plethora of pathological conditions are characterized by alterations in lipid metabolism, such as cardiovascular diseases and brain disorders. This Special Issue is a collection of papers from different experts in lipid research, with the aim of providing new insights into the physiopathological involvement of lipids and their impact on human health. This collection also demonstrates the usefulness of interdisciplinary approaches in the development of novel methods to study and manipulate lipid metabolism, which may represent an attractive target for designing effective therapeutic strategies to counteract numerous pathologies.

neutral sphingomyelinase --- radiation --- sphingomyelin metabolism --- pathology --- cell signaling --- brain --- adipose tissue --- breast cancer --- epinephrine --- breast reconstruction --- epicardial fat thickness --- visceral fat thickness --- high-sensitivity c-reactive protein --- leptin --- gender --- female --- hippocampus --- frontal cortex --- adiponectin --- haptoglobin --- lipocalin --- BDNF --- synaptic proteins --- phosphatidylinositol 4,5-bisphosphate --- phospholipase C --- cholesterol --- high-cholesterol diet --- BET proteins --- cell proliferation --- epigenetics --- HMGCR --- JQ1 --- LDLr --- lipid metabolism --- SREBP --- TMEM97 --- atherosclerosis --- diabetes mellitus --- cardiovascular disease --- chronic inflammation --- hyperglycemia --- mutations --- lipid --- fatty acid --- glyceride --- steroid --- phospholipid --- oral drug absorption --- prodrug --- phospholipase A2 (PLA2) --- acid sphingomyelinase --- SOD --- liver --- eicosanoids --- ischemic stroke --- ischemia --- lipoproteins --- polyunsaturated fatty acids --- angiogenesis --- high-density lipoprotein --- endothelial cell --- metabolism --- metabolic reprogramming --- pulmonary fibrosis --- lipid mediators --- sphingolipids --- sphingosine-1-phosphate --- sphingosine kinase 1 --- prostaglandins --- lysophosphatidic acid --- autotaxin --- G-protein coupled receptors --- lysocardiolipin acyltransferase --- phospholipase D --- oxidized phospholipids --- DNA damage response --- double strand breaks --- ATM --- ionizing radiation --- metabolic stress --- oxidative stress --- p53 --- nuclear sphingolipids --- lipophagy --- lipolysis --- lipid droplets --- lipid storage diseases --- lipid metabolism diseases --- mTORC1 --- TFEB --- Cholesterol --- Fatty acids --- Lipid mediators --- Lipids --- Lipophagy --- Sphingolipids