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The group of pattern recognition receptors (PRRs) includes families of Toll-like receptors (TLRs), NOD-like receptors (NLRs), C-type lectin receptors (CLRs), RIG-I-like receptors (RLRs), and AIM-2-like receptors (ALRs). Conceptually, receptors constituting these families are united by two general features. Firstly, they directly recognize common antigen determinants of virtually all classes of pathogens (so-called pathogen-associated molecular patterns, or simply PAMPs) and initiate immune response against them via specific intracellular signaling pathways. Secondly, they recognize endogenous ligands (since they are usually released during cell stress, they are called damage-associated molecular patterns, DAMPs), and, hence, PRR-mediated immune response can be activated without an influence of infectious agents. So, pattern recognition receptors play the key role performing the innate and adaptive immune response. In addition, many PRRs have a number of other vital functions apart from participation in immune response realization. The fundamental character and diversity of PRR functions have led to amazingly rapid research in this field. Such investigations are very promising for medicine as immune system plays a key role in vast majority if not all human diseases, and the process of discovering the new aspects of the immune system functioning is rapidly ongoing. The role of Toll-like receptors in cancer was analyzed in certain reviews but the data are still scattered. This collection of reviews systematizes the key information in the field.

Toll-Like Receptors --- C-type lectin receptors --- nod-like receptors --- DNA Repair --- Pattern Recognition Receptors --- Inflammation --- RIG-I-like receptors --- Autophagy --- Cancer --- Apoptosis

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Endotoxins are potentially toxic compounds produced by Gram-negative bacteria including some pathogens. Unlike exotoxins, which are secreted in soluble form by live bacteria, endotoxins are comprised of structural components of bacteria. Endotoxins can cause a whole-body inflammatory state, sepsis, leading to low blood pressure, multiple organ dysfunction syndrome and death. This book brings together contributions from researchers in the forefront of these subjects. It is divided into two sections. The first deals with how endotoxins are synthesized and end up on the bacterial surface. The second discussed how endotoxins activate TLR4 and, in turn, how TLR4 generates the molecular signals leading to infectious and inflammatory diseases. The way endotoxins interact with the host cells is fundamental to understanding the mechanism of sepsis, and recent research on these aspects of endotoxins has served to illuminate previously undescribed functions of the innate immune system. This volume presents a description of endotoxins according to their genetic constitution, structure, function and mode of interaction with host cells.

Endotoxins -- Pathophysiology. --- Endotoxins. --- Septic shock -- Molecular aspects. --- Endotoxins --- Septic shock --- Biological Science Disciplines --- Toll-Like Receptors --- Bacterial Toxins --- Receptors, Pattern Recognition --- Toxins, Biological --- Natural Science Disciplines --- Physiology --- Toll-Like Receptor 4 --- Receptors, Immunologic --- Disciplines and Occupations --- Biological Factors --- Receptors, Cell Surface --- Chemicals and Drugs --- Membrane Proteins --- Proteins --- Amino Acids, Peptides, and Proteins --- Biology --- Human Anatomy & Physiology --- Health & Biological Sciences --- Microbiology & Immunology --- Animal Biochemistry --- Pathophysiology --- Molecular aspects --- Bacterial pyrogens --- Endotoxin --- Lipopolysaccharides, Microbial --- Microbial lipopolysaccharides --- Medicine. --- Immunology. --- Medical microbiology. --- Pharmacology. --- Infectious diseases. --- Biomedicine. --- Medical Microbiology. --- Infectious Diseases. --- Pharmacology/Toxicology. --- Bacterial cell walls --- Bacterial toxins --- Gram-negative bacteria --- Microbial lipids --- Microbial polysaccharides --- Pyrogens --- Microbiology. --- Emerging infectious diseases. --- Toxicology. --- Immunobiology --- Life sciences --- Serology --- Chemicals --- Medicine --- Pharmacology --- Poisoning --- Poisons --- Emerging infections --- New infectious diseases --- Re-emerging infectious diseases --- Reemerging infectious diseases --- Communicable diseases --- Microbial biology --- Microorganisms --- Toxicology --- Drug effects --- Medical pharmacology --- Medical sciences --- Chemotherapy --- Drugs --- Pharmacy --- Physiological effect

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Our common knowledge on oxidative stress has evolved substantially over the years and has been mostly focused on the fundamental chemical reactions and the most relevant chemical species involved in the human pathophysiology of oxidative stress-associated diseases. Thus, reactive oxygen species and reactive nitrogen species (ROS and RNS) were identified as the key players initiating, mediating, and regulating the cellular and biochemical complexity of oxidative stress either as physiological (acting pro-hormetic) or as pathogenic (causing destructive vicious circle) process. The papers published in this particular Special Issue of the Cells demonstrate the impressive pathophysiological relevance of ROS and RNS in a range of contexts, including the relevance of second messengers of free radicals like 4-hydroxynonenal, allowing us to assume that even more detailed mechanisms of their positive and negative effects lie in wait, and should assist in better monitoring of the major modern diseases and the development of advanced integrative biomedicine treatments.

toxicity --- toll-like receptors --- acrolein --- hydroxyapatite-based biomaterials --- LC-MS/MS --- blood–brain barrier --- NADPH-oxidase --- human neuroblastoma SH-SY5Y cells --- NRF2-NQO1 axis --- granulocytes --- free radicals --- antioxidant --- plaque vulnerability --- bEnd.3 --- relaxation --- Ca2+ --- keratinocytes --- oxidative metabolism of the cells --- lipid peroxidation --- intermittent hypoxia --- osteoblast growth --- UV radiation --- ROS --- bEnd5 --- cyclopurines --- NF?B --- glucose deprivation --- antimicrobial --- endothelial cells --- 4-hydroxynonenal (4-HNE) --- histamine --- glutamine deprivation --- optical coherence tomography --- antioxidants --- DNA damage --- glutathione --- NQO1 transcript variants --- xeroderma pigmentosum --- cancer cells --- VAS2870 --- reactive oxygen species (ROS) --- TP53 mutation --- DNA and RNA polymerases --- viability --- oxidative burst --- macrophages --- inflammation --- Nrf2 --- von Willebrand factor --- reactive oxygen species --- growth control --- intracellular signaling --- MFN2 --- nuclear factor erythroid 2–related factor 2 --- fusion/fission --- IMR-90 --- calcium --- proliferation --- mitochondria --- pathophysiology of oxidative stress --- redox balance --- 4-hydroxynonenal --- cannabidiol --- oxidative homeostasis --- rs1800566 --- neuronal cell death --- heme-oxygenase-1 --- vitamins --- cell signaling --- TRPM2 channel --- aorta --- cancer --- growth --- cancer regression --- oxidative stress --- nucleotide excision repair

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Creatine plays a critical role in cellular metabolism, primarily by binding with phosphate to form phosphocreatine (PCr) as well as shuttling high-energy phosphate compounds in and out of the mitochondria for metabolism. Increasing the dietary availability of creatine increases the tissue and cellular availability of PCr, and thereby enhances the ability to maintain high-energy states during intense exercise. For this reason, creatine monohydrate has been extensively studied as an ergogenic aid for exercise, training, and sport. Limitations in the ability to synthesize creatine and transport and/or store dietary creatine can impair metabolism and is a contributor to several disease states. Additionally, creatine provides an important source of energy during metabolically stressed states, particularly when oxygen availability is limited. Thus, researchers have assessed the role of creatine supplementation on health throughout the lifespan, as well as whether creatine availability may improve disease management and/or therapeutic outcomes. This book provides a comprehensive overview of scientific and medical evidence related to creatine's role in metabolism, health throughout the lifespan, and our current understanding of how creatine can promote brain, heart, vascular and immune health; reduce the severity of musculoskeletal and brain injury; and may provide therapeutic benefits in glucose management and diabetes, cancer therapy, inflammatory bowel disease, and post-viral fatigue.

ergogenic aids --- cellular metabolism --- phosphagens --- sarcopenia --- cognition --- diabetes --- creatine synthesis deficiencies --- concussion --- traumatic brain injury --- spinal cord injury --- muscle atrophy --- rehabilitation --- pregnancy --- immunity --- anti-inflammatory --- antioxidant --- anticancer --- creatine --- nutritional supplements --- fertility --- newborn --- development --- brain injury --- post-viral fatigue syndrome --- chronic fatigue syndrome --- GAA --- creatine kinase --- dietary supplements --- exercise --- skeletal muscle --- glycemic control --- type 2 diabetes mellitus --- phosphorylcreatine --- dietary supplement --- ergogenic aid --- youth --- athletes --- osteoporosis --- osteosarcopenia --- frailty --- cachexia --- innate immunity --- adaptive immunity --- inflammation --- macrophage polarization --- cytotoxic T cells --- toll-like receptors --- vascular pathology --- cardiovascular disease --- oxidative stress --- vascular health --- female --- menstrual cycle --- hormones --- exercise performance --- menopause --- mood --- children --- height --- BMI-for-age --- stature-for-age --- growth --- phosphocreatine --- creatine transporter --- supplementation --- treatment --- heart --- heart failure --- ischemia --- myocardial infarction --- anthracycline --- cardiac toxicity --- energy metabolism --- cell survival --- bioinformatics --- systems biology --- cellular allostasis --- dynamic biosensor --- pleiotropic effects of creatine (Cr) supplementation --- inflammatory bowel diseases (IBD) --- ulcerative colitis --- Crohn’s disease --- creatine kinase (CK) --- phosphocreatine (PCr) --- creatine transporter (CrT) --- intestinal epithelial cell protection --- intestinal tissue protection --- creatine perfusion --- organ transplantation --- Adenosine mono-phosphate (AMP) --- activated protein kinase (AMPK) --- liver kinase B1 (LKB1) --- mitochondrial permeability transition pore (mPTP) --- reactive oxygen species (ROS) --- glucose transporter (GLUT) --- T cell antitumor immunity --- metabolic regulator --- cancer immunotherapy --- supplements --- muscle damage --- recovery --- immobilization --- atrophy --- muscular dystrophy --- amyotrophic lateral sclerosis --- Parkinson’s Disease --- cardiopulmonary disease --- mitochondrial cytopathy --- hypertrophy --- athletic performance --- weightlifting --- resistance exercise --- training --- muscular power --- muscular adaptation --- muscle fatigue --- adipose tissue --- muscle strength --- physiological adaptation --- mitochondria --- thermogenesis --- MAP kinase signaling system --- sodium-chloride-dependent neurotransmitter symporters --- signal transduction --- intradialytic creatine supplementation --- hemodialysis --- muscle --- protein energy wasting --- clinical trial --- muscle weakness --- chronic fatigue --- cognitive impairment --- depression --- anemia --- resistance training --- sports nutrition --- strength --- toxicity --- methylation --- hyperhomocysteinemia --- neuromodulation --- MCDA --- mitochondriopathia --- cardiac infarction --- long COVID --- hypoxia --- stroke --- neurodegenerative diseases --- noncommunicable disease --- adenosine 5′-monopnophosphate-activated protein kinase --- anthracyclines --- creatine supplementation --- cardiac signaling --- cardiotoxicity --- doxorubicin --- soy --- vegetarian/vegan diet --- amino acids --- dietary ingredients --- performance