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Pseudorabies virus (PRV) is an important swine pathogen that impacts swine industry worldwide. PRV belongs to the alphaherpes virus subfamily of the herpesviruses that has been widely used as a model herpes virus. Most recently, PRV has been reported sporadically spillover into human and other animals. This book collects the newest advances in the field of pseudorabies virus research, including critical reviews and research on viral evolution, replication, virus–host interaction, pathogenesis and immunity, and novel antiviral strategies.

Research & information: general --- Biology, life sciences --- Microbiology (non-medical) --- pseudorabies virus --- Liver X receptors --- clathrin-coated pits --- viral entry --- innate immune response --- type I interferons --- apoptosis --- autophagy --- premature termination codon --- genetic code expansion --- virus isolation --- pathogenicity --- mortality --- inflammatory response --- Huaier polysaccharide --- antiviral --- infection --- Vero cell --- TMT-based proteomic analysis --- differentially expressed proteins --- antiviral breeding --- genetic modification --- nectin1 --- pig --- PRV --- disease resistance --- seroprevalence --- epidemiology --- phylogenetic analysis --- variants --- ICP0 protein --- P65 --- NF-κB signaling pathway --- complete genome sequencing --- gene recombination --- variant strain --- genomics --- vaccination --- transmission --- zoonosis --- itch --- mouse --- histamine --- dorsal root ganglion --- metabolomic analysis --- UHPLC-QE-MS --- PK-15 cells --- latent infection --- latency-associated transcripts --- non-coding RNA --- latency --- miRNA --- chromatin --- immune regulation --- variation --- human pseudorabies encephalitis --- pseudorabies virus (PRV) --- tegument protein UL13 --- RIG-I --- MDA5 --- NF-κB --- pathogenesis --- prevention and control --- Aujeszky’s disease --- epidemiological characteristics

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This book contains research articles on the advances in the aetiology of idiopathic scoliosis (IS), the spinal growth related to the implementation of growth modulation for the surgical treatment of early-onset IS, the non-surgical treatment of IS using Physiotheraputic Scoliosis Specific Exercises, and braces. Additionally, it focuses on issues related to surgical treatment, issues related to body posture and the quality of life of this sensitive group of people. The high quality of published papers in this Special Issue of the JCM serve these objectives.

Medicine --- idiopathic scoliosis --- health-related quality of life --- cultural adaptation --- Italian Spine Youth Quality of Life Questionnaire --- systematic review --- meta-analysis --- adolescent idiopathic scoliosis --- brace therapy --- brace concepts --- rigid brace --- night time brace --- ring apophysis --- maturation --- ossification --- fusion --- scoliosis --- nighttime orthotic treatment --- surgery --- quality of life --- paraspinal muscles --- cross-sectional area --- posterior approach --- computed tomography --- Italian spine youth quality of life questionnaire --- SRS-22 --- 22q11.2 deletion syndrome --- human model --- neuromuscular scoliosis --- radiography --- MRI --- curve morphology --- intraspinal anomaly --- body height --- pulmonary function test --- Cobb angle --- iTRAQ --- α-actin --- progressive --- differentially expressed proteins --- bracing --- physiotherapeutic scoliosis-specific exercise --- physical activity --- adherence --- spinal appearance --- shared decision-making --- personalised approach --- sclerostin --- osteocytes --- β-catenin --- Wnt signaling pathway --- scoliometer --- truncal asymmetry --- lateral spinal profile --- surface topography --- aetiology --- spinal deformities --- pathobiomechanics --- follow-up study --- Rett syndrome --- motor skills --- telerehabilitation --- physical therapy modalities --- home exercise program --- neurodynamic functions --- assessment --- pain --- treatment --- early onset scoliosis --- non-operative treatment --- body posture --- sports activity --- corrective exercises --- digital photography --- n/a

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This book includes some recent works providing the readers with novel relevant findings about the main signaling pathways that govern the molecular pathogenesis of some of the highest prevalent human tumors, which are the basis for developing alternative therapeutic strategies to improve patient outcomes.

Medicine --- Oncology --- actin cytoskeletal reorganization --- breast cancer --- CD99 agonist --- EGFR dimerization --- endocytosis --- FAK dephosphorylation --- PTPN12 --- Rac1 --- RhoA --- tripeptide --- OMD --- PRELP --- tumor suppression gene --- bladder cancer initiation --- tight junction --- partial EMT --- tousled-like kinase (TLK) --- NIMA-related kinase 1 (NEK1) --- yes-associated protein 1 (YAP1) --- thioridazine (THD) --- MS-determined phosphopeptides --- human immunodeficiency virus type 1 --- epithelial cells --- carcinogenicity --- oxidative stress --- reactive oxygen species --- gp120 --- Tat --- Nef --- matrix protein p17 --- reverse transcriptase --- mitochondria --- metastasis --- OXPHOS --- cancer --- Warburg effect --- cancer therapeutics --- myeloproliferative neoplasms --- signaling pathways --- JAK2 --- CALR --- MPL --- TPOR --- DUSP1 --- MAPK --- Snail --- prostate cancer --- migration and invasion --- patient survival --- biomarkers --- pBRD4 --- SET --- PP2A --- prognosis --- triple negative breast cancer --- resistance --- anti-receptor therapy --- trastuzumab --- PI3K --- mTOR --- TAK-228 --- epigenetic --- methylation --- acetylation --- non-coding RNA --- small-cell lung cancer --- triple-negative breast cancer --- pancreatic ductal adenocarcinoma --- glioblastoma --- metastatic melanoma --- advanced ovarian cancer --- hepatocellular carcinoma --- immune evasion --- immunotherapy --- immune checkpoint inhibitors --- oncogenic signaling pathway --- molecular targeted agents --- genome --- epigenome --- tumor immune microenvironment --- ovarian cancer --- adaptive immunity --- innate immunity --- complement system --- cancer immunology --- tumor microenvironment --- splicing pathway --- luminal breast cancer --- BET inhibitors --- n/a

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Mounting evidence suggests a bidirectional relationship between metabolism and inflammation. Molecular crosstalk between these processes occurs at different levels with the participation of nuclear receptors, including peroxisome proliferator-activated receptors (PPARs). There are three PPAR isotypes, α, β/δ, and γ, which modulate metabolic and inflammatory pathways, making them key for the control of cellular, organ, and systemic processes. PPAR activity is governed by fatty acids and fatty acid derivatives, and by drugs used in clinics (glitazones and fibrates). The study of PPAR action, also modulated by post-translational modifications, has enabled extraordinary advances in the understanding of the multifaceted roles of these receptors in metabolism, energy homeostasis, and inflammation both in health and disease. This Special Issue of IJMS includes a broad range of basic and translational article, both original research and reviews, focused on the latest developments in the regulation of metabolic and/or inflammatory processes by PPARs in all organs and the microbiomes of different vertebrate species.

nuclear receptor --- gene transcription --- inflammation --- molecular docking --- PPARβ/δ --- lung --- pulmonary artery --- GW0742 --- GSK3787 --- docking --- lipopolysaccharide (LPS) --- PPARγ ligand --- coumarin --- fluorescent ligand --- screening --- crystal structure --- PPAR --- atopic dermatitis --- psoriasis --- metabolic reprograming --- glucose --- fatty acids --- mycobacteria --- M. tuberculosis --- M. leprae --- PPARs --- lipid droplets --- metabolic alterations --- hepatic damage --- nuclear factors --- pharmacological targets --- AMPK --- GDF15 --- insulin resistance --- type 2 diabetes mellitus --- peroxisome proliferator-activated receptor gamma (PPARγ) --- real-time PCR --- ELISA --- immunohistochemistry --- signaling pathway --- PPAR gamma --- brain --- neural stem cells --- infection --- neuroinflammation --- HIV --- Zika --- cytomegalovirus --- neurogenesis --- microglia --- liver damage --- toll-like receptor 4 --- P2Y2 receptor --- metabolic syndrome --- resveratrol --- quercetin --- PPARα --- peroxisome --- β-oxidation --- PPRE --- ligand --- coregulator --- micronutrients --- PPARα knockout --- adipose tissue --- browning --- lipid metabolism --- depression --- PPARg --- neuropathology --- corticotropin releasing hormone --- norepinephrine --- subgenual prefrontal cortex --- amygdala --- nucleus accumbens --- common carotid artery occlusion --- electroretinography --- fibroblast growth factor 21 --- pemafibrate --- peroxisome proliferator-activated receptor alpha --- retinal ischemia --- skeletal muscle --- substrate metabolism --- nonalcoholic fatty liver disease (NAFLD) --- sex dimorphism --- lipidomics --- hepatic sex-biased gene expression --- PPARγ --- pulmonary arterial hypertension --- TGFβ --- vascular injury --- proliferation --- kidney fibrosis --- pattern-recognition receptors --- phagocytosis --- nitric oxide synthase --- fenofibrate --- oleoylethanolamide --- palmitoylethanolamide --- cancer --- immunity --- obesity --- diabetes --- miRNA --- DNA methylation --- histone modification --- peroxisome-proliferator-activated receptor --- fatty acid oxidation --- doping control --- regulatory T cells --- exercise --- nuclear receptors --- nutrigenomics --- energy homeostasis --- dairy animals --- non-alcoholic fatty liver disease (NAFLD) --- non-alcoholic steatohepatitis (NASH) --- peroxisome proliferator-activated receptors (PPAR) --- bezafibrate --- fenofibric acid --- peroxisome proliferator-activated receptor --- dual/pan agonist --- X-ray crystallography --- n/a

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Mounting evidence suggests a bidirectional relationship between metabolism and inflammation. Molecular crosstalk between these processes occurs at different levels with the participation of nuclear receptors, including peroxisome proliferator-activated receptors (PPARs). There are three PPAR isotypes, α, β/δ, and γ, which modulate metabolic and inflammatory pathways, making them key for the control of cellular, organ, and systemic processes. PPAR activity is governed by fatty acids and fatty acid derivatives, and by drugs used in clinics (glitazones and fibrates). The study of PPAR action, also modulated by post-translational modifications, has enabled extraordinary advances in the understanding of the multifaceted roles of these receptors in metabolism, energy homeostasis, and inflammation both in health and disease. This Special Issue of IJMS includes a broad range of basic and translational article, both original research and reviews, focused on the latest developments in the regulation of metabolic and/or inflammatory processes by PPARs in all organs and the microbiomes of different vertebrate species.

Research & information: general --- Biology, life sciences --- Biochemistry --- nuclear receptor --- gene transcription --- inflammation --- molecular docking --- PPARβ/δ --- lung --- pulmonary artery --- GW0742 --- GSK3787 --- docking --- lipopolysaccharide (LPS) --- PPARγ ligand --- coumarin --- fluorescent ligand --- screening --- crystal structure --- PPAR --- atopic dermatitis --- psoriasis --- metabolic reprograming --- glucose --- fatty acids --- mycobacteria --- M. tuberculosis --- M. leprae --- PPARs --- lipid droplets --- metabolic alterations --- hepatic damage --- nuclear factors --- pharmacological targets --- AMPK --- GDF15 --- insulin resistance --- type 2 diabetes mellitus --- peroxisome proliferator-activated receptor gamma (PPARγ) --- real-time PCR --- ELISA --- immunohistochemistry --- signaling pathway --- PPAR gamma --- brain --- neural stem cells --- infection --- neuroinflammation --- HIV --- Zika --- cytomegalovirus --- neurogenesis --- microglia --- liver damage --- toll-like receptor 4 --- P2Y2 receptor --- metabolic syndrome --- resveratrol --- quercetin --- PPARα --- peroxisome --- β-oxidation --- PPRE --- ligand --- coregulator --- micronutrients --- PPARα knockout --- adipose tissue --- browning --- lipid metabolism --- depression --- PPARg --- neuropathology --- corticotropin releasing hormone --- norepinephrine --- subgenual prefrontal cortex --- amygdala --- nucleus accumbens --- common carotid artery occlusion --- electroretinography --- fibroblast growth factor 21 --- pemafibrate --- peroxisome proliferator-activated receptor alpha --- retinal ischemia --- skeletal muscle --- substrate metabolism --- nonalcoholic fatty liver disease (NAFLD) --- sex dimorphism --- lipidomics --- hepatic sex-biased gene expression --- PPARγ --- pulmonary arterial hypertension --- TGFβ --- vascular injury --- proliferation --- kidney fibrosis --- pattern-recognition receptors --- phagocytosis --- nitric oxide synthase --- fenofibrate --- oleoylethanolamide --- palmitoylethanolamide --- cancer --- immunity --- obesity --- diabetes --- miRNA --- DNA methylation --- histone modification --- peroxisome-proliferator-activated receptor --- fatty acid oxidation --- doping control --- regulatory T cells --- exercise --- nuclear receptors --- nutrigenomics --- energy homeostasis --- dairy animals --- non-alcoholic fatty liver disease (NAFLD) --- non-alcoholic steatohepatitis (NASH) --- peroxisome proliferator-activated receptors (PPAR) --- bezafibrate --- fenofibric acid --- peroxisome proliferator-activated receptor --- dual/pan agonist --- X-ray crystallography