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The present Special Issue summarizes the available scientific evidence concerning the nutrients and biomarkers in musculoskeletal diseases linked to the metabolic conditions secondary to COVID-19 confinement, osteoporosis prevention for patients with inflammatory bowel diseases, and the nutritional status in patients with spinal muscular atrophy. Furthermore, it explores the novel findings for experimental animal models of pharmacological agents to improve the regeneration of muscle tissue; acetylcholine spontaneous release located in the neuromuscular junction in mice, secondary to hypercaloric diet supplementation with an increase in spontaneous neurotransmission and the activation of myofascial trigger points associated with myofascial pain syndrome; and myogenic biomarkers in musculoskeletal conditions and gene expression associated with vitamin D and L-cysteine co-supplementation. This Special Issue is edited by a multidisciplinary group comprising the Universidad Complutense de Madrid, Universidad Rey Juan Carlos, Universidade da Coruña, and Universidad Europea de Madrid.

Humanities --- Social interaction --- COVID-19 --- acute sedentary lifestyle --- step reduction --- positive energy balance --- metabolic consequences --- insulin resistance --- metabolic syndrome --- sarcopenia --- bowel diseases --- diet --- osteoporosis --- bone density --- nutrients --- muscle unloading --- muscle reloading --- sirtuin-1 --- muscle progenitor cells --- activated satellite cells --- quiescent satellite cells --- muscle regeneration markers --- electromyography --- high-fat diet --- myofascial pain syndrome --- obesity --- spontaneous neurotransmission --- vitamin D deficiency --- l-cysteine --- glutathione --- myogenic markers --- dystrophy markers --- skeletal muscle --- spinal muscular atrophy --- metabolomics --- nutrition --- therapeutics --- biomarkers --- COVID-19 --- acute sedentary lifestyle --- step reduction --- positive energy balance --- metabolic consequences --- insulin resistance --- metabolic syndrome --- sarcopenia --- bowel diseases --- diet --- osteoporosis --- bone density --- nutrients --- muscle unloading --- muscle reloading --- sirtuin-1 --- muscle progenitor cells --- activated satellite cells --- quiescent satellite cells --- muscle regeneration markers --- electromyography --- high-fat diet --- myofascial pain syndrome --- obesity --- spontaneous neurotransmission --- vitamin D deficiency --- l-cysteine --- glutathione --- myogenic markers --- dystrophy markers --- skeletal muscle --- spinal muscular atrophy --- metabolomics --- nutrition --- therapeutics --- biomarkers

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The present Special Issue summarizes the available scientific evidence concerning the nutrients and biomarkers in musculoskeletal diseases linked to the metabolic conditions secondary to COVID-19 confinement, osteoporosis prevention for patients with inflammatory bowel diseases, and the nutritional status in patients with spinal muscular atrophy. Furthermore, it explores the novel findings for experimental animal models of pharmacological agents to improve the regeneration of muscle tissue; acetylcholine spontaneous release located in the neuromuscular junction in mice, secondary to hypercaloric diet supplementation with an increase in spontaneous neurotransmission and the activation of myofascial trigger points associated with myofascial pain syndrome; and myogenic biomarkers in musculoskeletal conditions and gene expression associated with vitamin D and L-cysteine co-supplementation. This Special Issue is edited by a multidisciplinary group comprising the Universidad Complutense de Madrid, Universidad Rey Juan Carlos, Universidade da Coruña, and Universidad Europea de Madrid.

COVID-19 --- acute sedentary lifestyle --- step reduction --- positive energy balance --- metabolic consequences --- insulin resistance --- metabolic syndrome --- sarcopenia --- bowel diseases --- diet --- osteoporosis --- bone density --- nutrients --- muscle unloading --- muscle reloading --- sirtuin-1 --- muscle progenitor cells --- activated satellite cells --- quiescent satellite cells --- muscle regeneration markers --- electromyography --- high-fat diet --- myofascial pain syndrome --- obesity --- spontaneous neurotransmission --- vitamin D deficiency --- l-cysteine --- glutathione --- myogenic markers --- dystrophy markers --- skeletal muscle --- spinal muscular atrophy --- metabolomics --- nutrition --- therapeutics --- biomarkers --- n/a

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Iron–sulfur (FeS) centers are essential protein cofactors in all forms of life. They are involved in many key biological processes. In particular, Fe-S centers not only serve as enzyme cofactors in catalysis and electron transfer, they are also indispensable for the biosynthesis of complex metal-containing cofactors. Among these cofactors are the molybdenum (Moco) and tungsten (Wco) cofactors. Both Moco/Wco biosynthesis and Fe-S cluster assembly are highly conserved among all kingdoms of life. After formation, Fe-S clusters are transferred to carrier proteins, which insert them into recipient apo-proteins. Moco/Wco cofactors are composed of a tricyclic pterin compound, with the metal coordinated to its unique dithiolene group. Moco/Wco biosynthesis starts with an Fe-S cluster-dependent step involving radical/S-adenosylmethionine (SAM) chemistry. The current lack of knowledge of the connection of the assembly/biosynthesis of complex metal-containing cofactors is due to the sheer complexity of their synthesis with regard to both the (genetic) regulation and (chemical) metal center assembly. Studies on these metal-cofactors/cofactor-containing enzymes are important for understanding fundamental cellular processes. They will also provide a comprehensive view of the complex biosynthesis and the catalytic mechanism of metalloenzymes that underlie metal-related human diseases.

CO dehydrogenase --- dihydrogen --- hydrogenase --- quantum/classical modeling --- density functional theory --- metal–dithiolene --- pyranopterin molybdenum enzymes --- fold-angle --- tungsten enzymes --- electronic structure --- pseudo-Jahn–Teller effect --- thione --- molybdenum cofactor --- Moco --- mixed-valence complex --- dithiolene ligand --- tetra-nuclear nickel complex --- X-ray structure --- magnetic moment --- formate hydrogenlyase --- hydrogen metabolism --- energy conservation --- MRP (multiple resistance and pH)-type Na+/H+ antiporter --- CCCP—carbonyl cyanide m-chlorophenyl-hydrazone --- EIPA—5-(N-ethyl-N-isopropyl)-amiloride --- nicotinamide adenine dinucleotide (NADH) --- electron transfer --- enzyme kinetics --- enzyme structure --- formate dehydrogenase --- carbon assimilation --- Moco biosynthesis --- Fe-S cluster assembly --- l-cysteine desulfurase --- ISC --- SUF --- NIF --- iron --- molybdenum --- sulfur --- tungsten cofactor --- aldehyde:ferredoxin oxidoreductase --- benzoyl-CoA reductase --- acetylene hydratase --- [Fe]-hydrogenase --- FeGP cofactor --- guanylylpyridinol --- conformational changes --- X-ray crystallography --- iron-sulfur cluster --- persulfide --- metallocofactor --- frataxin --- Friedreich’s ataxia --- n/a --- metal-dithiolene --- pseudo-Jahn-Teller effect --- CCCP-carbonyl cyanide m-chlorophenyl-hydrazone --- EIPA-5-(N-ethyl-N-isopropyl)-amiloride --- Friedreich's ataxia

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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