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The book starts with a review of the established facts on the numerical simulations of binary neutron star mergers and simulations of short GRB jets that highlights the issues that need to be revised and further clarified, as the need to understand how the relativistic outflow was launched, what the initial structure of the outflow is, and how it evolved through its interaction with the binary ejecta. Constraints on a local population of faint short duration GRBs are then provided in light of the GW170817/GRB 170817A event at d~40

galaxies --- host galaxies --- gamma-ray bursts --- gamma-ray burst --- GW170817 --- compact object mergers --- short GRBs --- prompt emission --- progenitors --- short gamma-ray bursts --- spectrum --- physics --- binary neutron stars

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The book is a collection of original research and review articles addressing the intriguing field of the cellular and molecular players involved in muscle homeostasis and regeneration. One of the most ambitious aspirations of modern medical science is the possibility of regenerating any damaged part of the body, including skeletal muscle. This desire has prompted clinicians and researchers to search for innovative technologies aimed at replacing organs and tissues that are compromised. In this context, the papers, collected in this book, addressing a specific aspects of muscle homeostasis and regeneration under physiopathologic conditions, will help us to better understand the underlying mechanisms of muscle healing and will help to design more appropriate therapeutic approaches to improve muscle regeneration and to counteract muscle diseases.

Research & information: general --- Biology, life sciences --- lysine --- mTORC1 --- satellite cells --- proliferation --- skeletal muscle growth --- muscle satellite cell --- transthyretin --- thyroid hormone --- myogenesis --- exosomes --- skeletal muscle --- genotype --- genetic variation --- muscle phenotypes --- sarcopenia --- aging --- calcium homeostasis --- hibernation --- mitochondria --- sarcoplasmic reticulum --- Acvr1b --- Tgfbr1 --- myostatin --- Col1a1 --- fibrosis --- atrophy --- IGF2R --- muscle homeostasis --- inflammation --- muscular dystrophy --- pericytes --- macrophages --- Nfix --- phagocytosis --- RhoA-ROCK1 --- splicing isoforms --- CRISPR-Cas9 --- exon deletion --- NF-Y --- muscle differentiation --- C2C12 cells --- denervation --- neuromuscular junction --- heavy resistance exercise --- acetylcholine receptor --- cell culture --- neonatal myosin --- neural cell adhesion molecule --- biomarkers --- mitophagy --- mitochondrial dynamics --- mitochondrial quality control --- mitochondrial-derived vesicles (MDVs) --- mitochondrial-lysosomal axis --- Hibernation --- electron microscopy --- immunocytochemistry --- α-smooth muscle actin --- confocal microscopy --- connexin 43 --- connexin 26 --- gap junctions --- myofibroblasts --- Platelet-Rich Plasma --- transforming growth factor (TGF)-β1 --- muscle regeneration --- inflammatory response --- cell precursors --- experimental methods --- stem cell markers --- muscles --- heterotopic ossification --- skeletal muscle stem and progenitor cells --- HO precursors --- muscle atrophy --- septicemia --- mitochondrial fusion --- mitochondrial fission --- iPSC --- extracellular vesicles --- Drosophila --- muscle --- genetic control --- muscle diversification --- fascicle --- myofiber --- myofibril --- sarcomere --- hypertrophy --- hyperplasia --- splitting --- radial growth --- longitudinal growth --- exercise --- muscle stem cells --- stem cells niche --- neuromuscular disorders --- Duchenne muscular dystrophy --- pharmacological approach --- single-cell --- mass cytometry --- skeletal muscle regeneration --- skeletal muscle homeostasis --- fibro/adipogenic progenitors --- myogenic progenitors --- muscle populations --- evolution --- metazoans --- differentiation --- transdifferentiation --- muscle precursors --- regenerative medicine --- stem cells --- FAPs --- tissue niche --- growth factors --- muscle pathology

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Nephropathic cystinosis (MIM # 219800) is a rare autosomal recessive disorder caused by mutations in the lysosomal cystine transporter cystinosin, encoded by the CTNS gene (17p13.2). This devastating condition initially affects kidneys and subsequently many other organs including eyes, thyroid, pancreas, muscles, and brain. While lysosomal cystine storage is a key feature of the disease and the main target of current therapy, recent groundbreaking research has revealed that cystinosin has diverse functions in cells, being involved in vesicle trafficking, energy homeostasis, and cell death mechanisms. These discoveries deepen our insights into the mechanisms of cystinosis and of lysosomal biology in general. In this Special Issue dedicated to the pioneer of cystinosis research Dr. Jerry Schneider, we highlight the state-of-the-art understanding of cellular and molecular mechanisms of various disease features, opening new horizons for innovative treatment strategies for cystinosis and potentially other lysosomal storage diseases.

Medicine --- Pharmacology --- cystinosis --- cysteamine --- bone --- osteoclast --- genotype --- CD34+ hematopoietic stem and progenitor cells --- gene therapy --- pre-clinical studies --- investigational new drug application --- clinical trial --- disulfiram --- mice --- zebrafish --- fertility --- azoospermia --- hypogonadism --- histopathology --- mouse model --- lysosomal storage disease --- cell and animal models --- infantile nephropathic cystinosis --- bone-muscle wasting --- fibroblast growth factor 23 --- osteoclasts --- sclerostin --- leptin --- fractures --- nephropathic cystinosis --- hollow fiber membrane --- 3-dimensional models --- autophagy --- macrophages --- inflammasome --- proximal tubular cells --- endocytosis --- apoptosis --- chitotriosidase --- interleukins --- galectin-3 --- novel therapies --- endolysosome --- epithelial cell differentiation --- homeostasis --- lysosomal storage diseases --- mitochondrial distress --- kidney proximal tubule --- programmed cell death --- central nervous system --- cortical atrophy --- arterial spin labelling --- cystine blood level --- lysosomal storage disorder --- history --- treatment strategies for cystinosis --- newborn screening --- clinical course --- CTNS-pathogenic variants --- newborn screening for cystinosis --- kidney progenitors --- cell model --- biomarkers --- cystine --- kidney --- therapeutic monitoring

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Acute kidney injury (AKI) is still associated with high morbidity and mortality incidence rates, and also bears an elevated risk of subsequent chronic kidney disease. Although the kidney has a remarkable capacity for regeneration after injury and may recover completely depending on the type of renal lesions, the options for clinical intervention are restricted to fluid management and extracorporeal kidney support. The development of novel therapies to prevent AKI, to improve renal regeneration capacity after AKI, and to preserve renal function is urgently needed. The Special Issue covers research articles that investigated the molecular mechanisms of inflammation and injury during different renal pathologies, renal regeneration, diagnostics using new biomarkers, and the effects of different stimuli like medication or bacterial components on isolated renal cells or in vivo models. The Special Issue contains important reviews that consider the current knowledge of cell death and regeneration, inflammation, and the molecular mechanisms of kidney diseases. In addition, the potential of cell-based therapy approaches that use mesenchymal stromal/stem cells or their derivates is summarized. This edition is complemented by reviews that deal with the current data situation on other specific topics like diabetes and diabetic nephropathy or new therapeutic targets.

microRNAs --- n/a --- transcription --- ischemia/reperfusion injury --- DSS-colitis --- kidney inflammation --- therapeutics targets --- CXCL13 --- glomerulus --- interleukin-6 --- rhabdomyolysis --- IgA nephropathy --- CREB Regulated Transcriptional Coactivators (CRTC) --- slit diaphragm --- injury --- xanthine oxidase --- Salt Inducible Kinase (SIK) --- acute and chronic kidney disease --- therapeutic target --- KIT-IgA score --- G-protein-coupled bile acid receptor (TGR5) --- lysophosphatidic acid --- glomerular injury --- IL-18 --- mesenchymal stem cells --- Taiwan --- acute kidney injury --- renal ischemia-reperfusion --- long non-coding RNA --- fibrosis --- acute kidney failure --- diabetic kidney diseases --- chronic kidney disease --- lncRNA --- LPS-binding protein --- endotoxemia-induced oliguric kidney injury --- dapagliflozin --- cPLA2 and COX-2 --- NLRP3 inflammasome --- CmklR1 --- haem --- chronic kidney injury --- omega-3 fatty acid --- noninvasive --- inflammation --- regulated necrosis --- GLP-1 receptor agonists --- miRNA --- AKI --- SGLT2 inhibitors --- diabetic kidney disease --- extracellular vesicles --- podocin --- type IV collagen --- epithelial cells --- nephrin --- 2-kidney-1-clip --- renal fibrosis --- papilla --- diagnostics --- necrosis --- non-coding RNAs --- podocyte --- Thy1.1 nephritis --- KIT assay --- oxidative stress --- conditioned medium --- C-reactive protein --- pericyte --- myofibroblast --- Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-?B) --- endotoxemia --- modifier gene --- polymorphism --- renal stem cells --- kidney --- polyploidization --- Class IIa Histone Deacetylases (HDAC) --- 2k1c --- molecular signaling --- proximal tubule --- arachidonic acid --- empagliflozin --- tubular injury --- signaling cascade --- signal transduction --- inflammatory maker --- niches --- biomarkers --- renal progenitors --- type V collagen --- cyclooxygenase --- focal segmental glomerulosclerosis --- inflammatory bowel disease (IBD) --- chronic kidney disease (CKD) --- allograft rejection --- renovascular hypertension --- genotype --- molecular mechanisms --- ROS --- prediction --- glomerular filtration barrier (GFB) --- alport syndrome --- scattered tubular cells --- long non-coding RNAs --- renal inflammation --- lysophosphatidic acid receptor --- cAMP Regulatory Element Binding Protein (CREB) --- Farnesiferol B --- differentiation --- mesenchymal stromal cells --- modified-MSCs --- kidney transplantation --- polyunsaturated fatty acids --- apoptosis --- type I collagen --- diabetes mellitus --- natural products --- lipoxygenase --- stem cell --- T cell-mediated rejection --- exosomes --- renal injury --- obese kidney fibrosis --- kidney injury --- cytotoxicity --- mesenchymal stem cell --- pigment nephropathy --- mesodermal stem cell --- ischemia-reperfusion --- cytochrome P450 --- renal cell carcinoma --- hematuria --- B-cell attracting chemokine --- microRNA --- chemerin --- glomerular basement membrane --- glomerular damage --- renal tubular cells --- kidney proximal tubule --- exosome --- hypertension --- diabetic nephropathy