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Salt (NaCl) is a key component of the human diet because it provides the sodium ion (Na+), an essential mineral for our body. Na+ regulates extracellular fluid volume and plays a key role in many physiological processes, such as the generation of nerve impulses. Na+ is lost continuously through the kidneys, intestine, and sweating. Thus, to maintain proper bodily balance, losses have to be balanced with foods containing this cation. The need for salt explains our ability to detect Na+ in foodstuffs: Na+ elicits a specific taste sensation called “salty”, and gustatory sensitivity to this cation is crucial for regulating its intake. Indeed, the widespread use of salt in food products for flavoring and to improve their palatability exploits our sense of taste for Na+. When consumed in excess, however, salt might be detrimental to health because it may determine an increase in blood pressure—a major risk factor for many cardiovascular diseases. Understanding how salt taste works and how it affects food preference and consumption is therefore of paramount importance for improving human nutrition. This book comprises cutting-edge research dealing with salt taste mechanisms relevant for nutrition and health.

taste sensitivity --- taste thresholds --- food records --- food intake --- oral microbiota --- eating habits --- taste --- sodium taste --- renin --- angiotensin II --- angiotensinogen --- angiotensin-converting enzyme --- high-salt diet --- blood pressure --- doenjang --- soybean paste --- epithelial sodium channel --- sodium homeostasis --- amiloride --- salt deprivation --- short-term preference test --- salt --- TRPV1 gene --- rs806500 --- dietary --- biomarker --- elderly --- nutrigenetics --- salt taste perception --- taste threshold --- sodium chloride --- metabolic syndrome --- Mediterranean diet --- sodium receptor --- salt taste --- taste transduction --- Korean soy sauce --- kokumi --- umami --- salty --- chorda tympani --- amiloride-insensitive salt taste pathway --- n/a

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Salt (NaCl) is a key component of the human diet because it provides the sodium ion (Na+), an essential mineral for our body. Na+ regulates extracellular fluid volume and plays a key role in many physiological processes, such as the generation of nerve impulses. Na+ is lost continuously through the kidneys, intestine, and sweating. Thus, to maintain proper bodily balance, losses have to be balanced with foods containing this cation. The need for salt explains our ability to detect Na+ in foodstuffs: Na+ elicits a specific taste sensation called “salty”, and gustatory sensitivity to this cation is crucial for regulating its intake. Indeed, the widespread use of salt in food products for flavoring and to improve their palatability exploits our sense of taste for Na+. When consumed in excess, however, salt might be detrimental to health because it may determine an increase in blood pressure—a major risk factor for many cardiovascular diseases. Understanding how salt taste works and how it affects food preference and consumption is therefore of paramount importance for improving human nutrition. This book comprises cutting-edge research dealing with salt taste mechanisms relevant for nutrition and health.

Research & information: general --- Biology, life sciences --- Food & society --- taste sensitivity --- taste thresholds --- food records --- food intake --- oral microbiota --- eating habits --- taste --- sodium taste --- renin --- angiotensin II --- angiotensinogen --- angiotensin-converting enzyme --- high-salt diet --- blood pressure --- doenjang --- soybean paste --- epithelial sodium channel --- sodium homeostasis --- amiloride --- salt deprivation --- short-term preference test --- salt --- TRPV1 gene --- rs806500 --- dietary --- biomarker --- elderly --- nutrigenetics --- salt taste perception --- taste threshold --- sodium chloride --- metabolic syndrome --- Mediterranean diet --- sodium receptor --- salt taste --- taste transduction --- Korean soy sauce --- kokumi --- umami --- salty --- chorda tympani --- amiloride-insensitive salt taste pathway --- n/a

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Dilated cardiomyopathy (DCM) is a particular phenotype of non-ischemic systolic heart failure, frequently recognizing a genetic background and affecting relatively young patients with few comorbidities. Nowadays, long-term survival of DCM patients has been markedly improved due to an early diagnosis and uninterrupted and tailored follow-up under constant optimal medical and non-pharmacological evidence-based treatments. Nevertheless, DCM is still one of the most common causes of heart transplantation in the western world. Clinical management requires an integrated and systematic use of diagnostic tools and a deeper investigation of the basic mechanisms underlying the disease. However, several emerging issues remain debated. Specifically, the genotype–phenotype correlation, the role of advanced imaging techniques and genetic testing, the lack of appropriate risk stratification models, the need for a multiparametric and multidisciplinary approach for device implantation, and a continuous reclassification of the disease during follow-up remain challenging issues in clinical practice. Therefore, the aim of this Special Issue is to shed the light on the most recent advancements in characterization and clinical management of DCM in order to unveil the conundrum of this particular disease.

Medicine --- SCN5A --- cardiac sodium channel --- cardiac channelopathy --- dilated cardiomyopathy --- precision medicine --- arrhythmias --- atrial fibrillation --- cardiomyopathy --- heart failure --- supraventricular arrhythmia --- systolic dysfunction --- tachycardiomyopathy --- ventricular arrhythmia --- left atrial strain --- cardiac resynchronization therapy --- muscular dystrophy --- calcium --- heart --- gene therapy --- phospholamban --- Serca2a --- mdx --- oxidative stress --- membrane stabilization --- left ventricular noncompaction --- congenital heart disease --- congestive heart failure --- non-ischemic cardiomyopathy --- genetics --- desmin --- mitochondrial dysfunction --- myopathy --- whole exome sequencing --- laminopathy --- LMNA --- biomarkers --- troponin T --- NT-proBNP --- malignant ventricular arrhythmia --- arrhythmic risk stratification --- DNA methylation --- alternative splicing --- epigenetics --- nonischemic dilated cardiomyopathy --- cardiac magnetic resonance imaging --- late gadolinium enhancement --- long axis strain --- left ventricle sphericity index --- major adverse cardiovascular events --- sex differences --- left ventricular reverse remodelling --- long-term outcomes --- left ventricle non-compaction cardiomyopathy --- cardiac magnetic resonance --- titin --- RNA binding motif protein 20 (RBM20) --- sarcomere --- diastolic dysfunction --- phosphorylation --- non-sense mRNA decay --- mammalian target of rapamycin (mTOR) complex-1 --- duchenne muscular distrophy --- n/a

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Ubiquitination is a biological process mediated by ubiquitin itself, the E1 ubiquitin-activating enzyme, E2 ubiquitin-conjugating enzyme, E3 ubiquitin ligase, and deubiquitinating enzyme, respectively. Currently, these multiple biological steps are revealed to participate in various life phenomena, such as cell proliferation, regulation of cell surface proteins expression, and mitochondrial function, which are profoundly related to human health and diseases. Although clinical applications targeting ubiquitination are still limited compared to those directed toward kinase systems such as tyrosine kinases, multiple enzymatic consequences should be future therapeutic implications. This Special Issue of IJMS entitled “Ubiquitination in Health and Disease” successfully published15 distinguished manuscripts, with a total of 66 international authors and. This book provides the latest and most useful information for researchers and scientists in this field.

Humanities --- Social interaction --- deubiquitinase --- degradation --- therapeutic target --- cancer --- hematopoiesis --- hematopoietic stem cells --- immune response --- regulation of gene expression --- ubiquitin system --- genetic diseases --- ubiquitin ligase --- deubiquitinases --- monoubiquitin signaling --- vesicular trafficking --- protein complex formation --- inflammation --- inhibitor --- innate immune --- interferon --- LUBAC --- NF-κB --- ubiquitin --- Parkinson’s disease --- dopa-responsive dystonia --- tyrosine hydroxylase --- α-synuclein --- fatty acid-binding protein 3 --- ubiquitination --- proteasomal degradation --- ubiquitin-proteasome system --- mitochondria --- E3 ubiquitin ligase --- MITOL/MARCH5 --- salt-sensitive hypertension --- Nedd4L/Nedd4-2 --- epithelial sodium channel --- aldosterone sensitive distal nephron --- excitation-transcription coupling --- RNF183 --- RNF186 --- RNF182 --- RNF152 --- RING finger --- mTOR --- endoplasmic reticulum stress --- osmotic stress --- ubiquitin code --- virus infection --- virus-host interaction --- tau protein --- semisynthesis --- disulfide-coupling --- polyubiquitin --- fibrils --- aggregation --- neurodegeneration --- deubiquitination --- inhibitors --- protein quality control --- proteolysis --- protein stabilization --- regulatory T cells --- mesenchymal stem cell --- cortical bone derived stem cell --- myocardial infarction --- blood pressure --- renal salt reabsorption --- vascular function --- ubiquitin proteasome system --- ubiquitin–proteasome pathway --- cilia --- ciliogenesis --- differentiation --- proliferation --- ciliopathy --- E3s --- DUBs --- UPS --- neurodegenerative disease --- immune-related diseases

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Dilated cardiomyopathy (DCM) is a particular phenotype of non-ischemic systolic heart failure, frequently recognizing a genetic background and affecting relatively young patients with few comorbidities. Nowadays, long-term survival of DCM patients has been markedly improved due to an early diagnosis and uninterrupted and tailored follow-up under constant optimal medical and non-pharmacological evidence-based treatments. Nevertheless, DCM is still one of the most common causes of heart transplantation in the western world. Clinical management requires an integrated and systematic use of diagnostic tools and a deeper investigation of the basic mechanisms underlying the disease. However, several emerging issues remain debated. Specifically, the genotype–phenotype correlation, the role of advanced imaging techniques and genetic testing, the lack of appropriate risk stratification models, the need for a multiparametric and multidisciplinary approach for device implantation, and a continuous reclassification of the disease during follow-up remain challenging issues in clinical practice. Therefore, the aim of this Special Issue is to shed the light on the most recent advancements in characterization and clinical management of DCM in order to unveil the conundrum of this particular disease.

SCN5A --- cardiac sodium channel --- cardiac channelopathy --- dilated cardiomyopathy --- precision medicine --- arrhythmias --- atrial fibrillation --- cardiomyopathy --- heart failure --- supraventricular arrhythmia --- systolic dysfunction --- tachycardiomyopathy --- ventricular arrhythmia --- left atrial strain --- cardiac resynchronization therapy --- muscular dystrophy --- calcium --- heart --- gene therapy --- phospholamban --- Serca2a --- mdx --- oxidative stress --- membrane stabilization --- left ventricular noncompaction --- congenital heart disease --- congestive heart failure --- non-ischemic cardiomyopathy --- genetics --- desmin --- mitochondrial dysfunction --- myopathy --- whole exome sequencing --- laminopathy --- LMNA --- biomarkers --- troponin T --- NT-proBNP --- malignant ventricular arrhythmia --- arrhythmic risk stratification --- DNA methylation --- alternative splicing --- epigenetics --- nonischemic dilated cardiomyopathy --- cardiac magnetic resonance imaging --- late gadolinium enhancement --- long axis strain --- left ventricle sphericity index --- major adverse cardiovascular events --- sex differences --- left ventricular reverse remodelling --- long-term outcomes --- left ventricle non-compaction cardiomyopathy --- cardiac magnetic resonance --- titin --- RNA binding motif protein 20 (RBM20) --- sarcomere --- diastolic dysfunction --- phosphorylation --- non-sense mRNA decay --- mammalian target of rapamycin (mTOR) complex-1 --- duchenne muscular distrophy --- n/a