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Neonatal and Pediatric Cerebro-Cardiopulmonary Resuscitation

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889456598 Year: Pages: 112 DOI: 10.3389/978-2-88945-659-8 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Pediatrics
Added to DOAB on : 2019-01-23 14:53:43
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Pediatric resuscitation medicine has witnessed significant advances with improved understanding of the pathophysiology of cardiac arrest and resuscitation. Multiple mechanisms of neurological injury have been identified, outlining potential avenues for neuroprotection following cardiac arrest. Resuscitation science exists at multiple levels of analysis, from biomechanics of chest compressions to implementation of best training procedures in real time, from epidemiology of cardiac arrest survival to molecular mechanisms of cellular injury due to ischemia and reperfusion. What next steps in research and in clinical practice will ensure the best possible neurologic outcome among children who survive cardiac arrest? How can we leverage novel technologies in neuroimaging, nanomaterials, drug delivery, biomarker-based risk stratification and next generation sequencing, among others, to resuscitate and to protect the Central Nervous System (CNS)? How can we improve clinical trial design and data analyses to maintain a robust clinical research infrastructure and to ensure validity and applicability? These are just some of the questions will addressed in this Research Topic. Using evidence-based algorithms and public health approaches to disseminate them, the last decade has seen a paradigm shift in pediatric resuscitation with significantly improved survival from pediatric cardiac arrests. However, neurologic outcome in survivors remains far from optimal. High quality CPR is increasingly recognized as a key factor for improving neurologic outcomes. Advanced technologies allow monitoring the quality of CPR and just-in-time feedback to improve the quality of CPR. Further research is needed to evaluate impact of these technologies on neurologic outcome. The recent American Heart Association CPR guidelines emphasis on Circulation-Airway-Breathing (CAB) approach to CPR needs a careful evaluation in children, in whom timely airway and breathing support are as important as circulation. The growing controversy regarding use of epinephrine, and alternative routes of administration of epinephrine during CPR, warrants further evaluation in the setting of pediatric CPR. Improved outcome of hemodynamic goal-directed CPR over standard CPR in animal models of cardiac arrest has initiated interest in physiology-based CPR, especially in the in-hospital cardiac arrest. Basic and applied-science research have become relevant for specific subpopulations of pediatric cardiac arrest victims and circumstances (e.g., ventricular fibrillation, neonates, congenital heart disease, extracorporeal cardiopulmonary resuscitation). Just-in-time and just-in-place simulation training, which have evolved as training strategies to improve quality of CPR, are being evaluated for outcomes. The concept of just-in-time and just-in-place coaching of CPR providers on high quality CPR is a novel concept which has emerged recently and remains unstudied. Whilst there have been significant advances in newborn stabilization over the last decade many questions remain unanswered. These include the role of delayed cord clamping in preterm infants and term newborns requiring resuscitation, the role of sustained inflations as a method of respiratory support and the role of epinephrine and volume administration in neonatal resuscitation. Novel methods of assessment including the use of end tidal CO2 monitoring, respiratory function monitoring and near infrared spectroscopy warrant further evaluation. The use of transitioning animal models that accurately replicate the newborn circulation with patent fetal shunts are emerging but more assessments in these are required to better establish CPR strategies in newborn infants. Newborn resuscitation training programs have resulted in a reduction in neonatal mortality in the developing world, but key questions remain around the frequency of training, team training methods and the role of simulation training. Post resuscitation interventions, in particular therapeutic hypothermia, has resulted in significant improvements in long-term outcome and there is now a growing interest in adjunct therapies, such as use of melatonin, erythropoietin, or other neuroprotective molecules to improve therapeutic benefits of cooling. Therapeutic hypothermia did not provide any higher benefit than normothermia in children following out of hospital cardiac arrest, although three is considerable debate in the community whether 14% probability of observing a similar outcome if the study were repeated a 100 times applies to an individual child in the PICU. Exciting research is occurring in unraveling connection between inflammation, immune dysregulation and neuroinjury. This will further support research on the use of anti-inflammatory agents and immunomodulators for neuroprotection after cardiac arrest and birth asphyxia.

Second hand smoke and COPD: lessons from animal studies

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193165 Year: Pages: 91 DOI: 10.3389/978-2-88919-316-5 Language: English
Publisher: Frontiers Media SA
Subject: Physiology --- Science (General)
Added to DOAB on : 2016-02-05 17:24:33
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Cigarette smoke exposure is the key initiator of chronic inflammation, alveolar destruction, and the loss of alveolar blood vessels that lead to the development of chronic obstructive pulmonary disease (COPD) which is comprised of emphysema and chronic bronchitis. Exposure to secondhand smoke (SHS) is the major risk factor for non-smokers to develop emphysema. While the first-hand smoke is directly inhaled by smokers, passive smoking occurs when non-smokers are involuntary exposed to environmental tobacco smoke also known as second hand smoke (SHS). SHS is a mixture of 2 forms of smoke that come from burning tobacco: side stream smoke (smoke that comes from the end of a lit cigarette, pipe, or cigar) and mainstream smoke (smoke that is exhaled by a smoker). These two types of smoke have basically the same composition, however in SHS many toxic components are more concentrated than in first-hand smoke, therefore more hazardous for people’s health. Several pathological events have been implicated in the development of SHS-induced COPD, but many aspects of this pathology remain poorly understood halting the development of new advanced treatments for this detrimental disease. In this respect we have welcomed leading investigators in the field to share their research findings and provide their thoughts regarding the mechanisms of the SHS exposure-induced immune responses and inflammatory mechanisms of lung destruction in SHS-induced COPD and related comorbidities.

Systems Biology Approaches to Understanding the Cause and Treatment of Heart, Lung, Blood, and Sleep Disorders

Authors: --- ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889192496 Year: Pages: 180 DOI: 10.3389/978-2-88919-249-6 Language: English
Publisher: Frontiers Media SA
Subject: Biotechnology --- General and Civil Engineering --- Physiology --- Science (General)
Added to DOAB on : 2015-11-16 15:44:59
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Development of powerful new high- throughput technologies for probing the transcriptome, proteome and metabolome is driving the rapid acquisition of information on the function of molecular systems. The importance of these achievements cannot be understated - they have transformed the nature of both biology and medicine. Despite this dramatic progress, one of the greatest challenges that continues to confront modern biology is to understand how behavior at the level of genome, proteome and metabolome determines physiological function at the level of cell, tissue and organ in both health and disease. Because of the inherent complexity of biological systems, the development, analysis, and validation of integrative computational models based directly on experimental data is necessary to achieve this understanding. This approach, known as systems biology, integrates computational and experimental approaches through iterative development of mathematical models and experimental validation and testing. The combination of these approaches allows for a mechanistic understanding of the function of complex biological systems in health and their dysfunction in disease. The National Heart, Lung, and Blood Institute (NHLBI) has recognized the importance of the systems biology approach for understanding normal physiology and perturbations associated with heart, lung, blood, and sleep diseases and disorders. In 2006, NHLBI announced the Exploratory Program in Systems Biology, followed in 2010 by the NHLBI Systems Biology Collaborations. The goal of these programs is to support collaborative teams of investigators in using experimental and computational strategies to integrate the component parts of biological networks and pathways into computational models that are based firmly on and validated using experimental data. These validated models are then applied to gain insights into the mechanisms of altered system function in disease, to generate novel hypotheses regarding these mechanisms that can be tested experimentally, and to then use the results of experiments to refine the models. The purpose of this Research Topic is to present the range of innovative, new approaches being developed by investigators working in areas of systems biology that couple experimental and modeling studies to understand the cause and possible treatment of heart, lung, blood and sleep diseases and disorders. This Research Topic will be of great interest to the cardiovascular research community as well as to the general community of systems biologists.

Recent Advances in Scar Biology

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ISBN: 9783038973980 / 9783038973997 Year: Pages: 202 DOI: 10.3390/books978-3-03897-399-7 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Biology --- Pathology --- Physiology
Added to DOAB on : 2019-01-29 11:30:03
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Scars develop in the final stage of wound healing. Wound healing and scarring involve complex biological pathways, and the exact mechanisms by which they are initiated, evolved, and regulated remain to be fully elucidated. Scarless wound healing is a major goal of medical science. To achieve this goal, it is necessary to elucidate the relevant clinical, histopathological, and molecular manifestations of scars, and to understand how these manifestations relate to each other.This Special Issue covers a selection of recent research topics and current review articles in the field of scar research for all kinds of tissues and organs.

Redox and Nitrosative Signaling in Cardiovascular System: From Physiological Response to Disease

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889457267 Year: Pages: 258 DOI: 10.3389/978-2-88945-726-7 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Physiology
Added to DOAB on : 2019-01-23 14:53:43
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The role of ROS/RNS signaling in cardiovascular functions and diseases is increasingly emerging in the last decades. The involvement of ROS/RNS in the control of a large number of cardiovascular functions like the regulation of the vascular tone, the control of blood pressure or myocyte excitation-contraction coupling and force development has been broadly investigated and in part clarified. On the other hand, many efforts have been focused in clarifying the redox mechanisms involved in cardiovascular diseases like ischemia/reperfusion injury, diabetes-associated cardiovascular dysfunctions, atherosclerosis or hypertension, just to mention the major ones. However, in most cases the two levels of investigation remain separate and not interlaced, failing in the attempt to provide a unified vision of the pathophysiologic mechanisms of cardiovascular diseases. The major aim of the Research Topic has been to collect original papers and review articles dealing with the issue from basic to translation research point of views. The topic includes contributions that highlight different interesting aspects of cardiovascular biology with an integrated approach useful for the development of new ideas and advancements in the field of redox signaling in the control of normal cardiovascular functions and their disruption in diseases.

Molecular Basis of Cardiovascular Diseases: Implications of Natriuretic Peptides

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ISBN: 9783039215829 / 9783039215836 Year: Pages: 212 DOI: 10.3390/books978-3-03921-583-6 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General) --- Cardiovascular
Added to DOAB on : 2019-12-09 11:49:16
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The natriuretic peptides (NPs) family includes a class of hormones and their receptors needed for the physiological control of cardiovascular functions. The discovery of NPs provided a fundamental contribution into our understanding of the physiological regulation of blood pressure, and of heart and kidney functions. NPs have also been implicated in the pathogenesis of several cardiovascular diseases (CVDs), including hypertension, atherosclerosis, heart failure, and stroke. A fine comprehension of the molecular mechanisms dependent from NPs and underlying the promotion of cardiovascular damage has contributed to improve our understanding of the molecular basis of all major CVDs. Finally, the opportunity to target NPs in order to develop new therapeutic tools for a better treatment of CVDs has been developed over the years. The current Special Issue of the Journal covers all major aspects of the molecular implications of NPs in physiology and pathology of the cardiovascular system, including NP-based therapeutic approaches.

Keywords

PCSK9 --- natriuretic peptides --- adipose tissue --- lipid metabolism --- LDL receptor --- insulin --- natriuretic peptides --- hypertension --- stroke --- cardiac hypertrophy --- linkage analysis --- genetic variants --- animal models --- BNP --- NT-proBNP --- heart failure --- cardiac dysfunction --- forensic medicine --- postmortem biochemistry --- angiotensin receptor–neprilysin inhibitor --- natriuretic peptides --- renin–angiotensin system --- heart failure --- arterial hypertension --- natriuretic peptide --- vascular --- endothelial cell --- cardiomyocyte --- fibroblast --- inflammation --- heart failure --- hypertension --- angiogenesis --- heart failure --- natriuretic peptides --- preserved ejection fraction --- natriuretic peptides --- heart failure --- atrial fibrillation --- remodeling --- Idiopathic Pulmonary Arterial Hypertension (IPAH) --- Natriuretic Peptide Clearance Receptor (NPR-C) signaling --- atrial natriuretic peptide --- hypertension --- heart failure --- cardiometabolic disease --- obesity --- metabolic syndrome --- cGMP --- guanylyl cyclase receptor A --- natriuretic peptides --- natriuretic peptide --- cardiorenal syndrome --- vasopressor --- vasodilator --- kidney --- medulla --- renin-angiotensin-aldosterone system --- Atrial Natriuretic peptide --- natriuretic peptides --- cardiac remodelling --- cardiac hypertrophy --- vascular homeostasis --- atrial natriuretic peptide --- guanylyl cyclase/natriuretic peptide receptor-A --- gene-knockout --- gene-duplication --- hypertension --- congestive heart failure --- natriuretic peptides --- arterial hypertension --- pulmonary arterial hypertension --- heart failure --- stroke --- atrial fibrillation --- ARNi --- MANP

Links between Fibrogenesis and Cancer: Mechanistic and Therapeutic Challenges: Mechanistic and Therapeutic Challenges

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ISBN: 9783039217069 / 9783039217076 Year: Pages: 348 DOI: 10.3390/books978-3-03921-707-6 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General) --- Internal medicine
Added to DOAB on : 2019-12-09 11:49:16
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Tissue fibrosis may occur for unknown causes or be the consequence of many pathological conditions including chronic inflammatory or infectious diseases, autoimmune disorders, graft rejection, or malignancy. On the other hand, malignant tumors have been identified in fibrotic tissues decades ago, and now accumulating evidence suggests that fibrotic lesions enhance the risk of cancer in several organs such as liver, lungs, and breast. Disruption of an organ parenchymal cells and of its normal structural scaffold during tissue fibrogenesis appears to induce loss of cell polarity, promoting uncontrolled cell proliferation that may eventually lead to cancer development. Many cellular and molecular abnormalities including aberrant expression of microRNAs, genetic and epigenetic alterations, evasion or delayed apoptosis, unregulated intracellular signal pathways, and dysregulation or defective intercellular communications have been proposed to explain this link between fibrogenesis and carcinogenesis. However, the precise mechanisms of this fibrosis-to-cancer transition remain unclear. This book presents a collection of reviews and original articles summarizing recent advances in understanding the molecular mechanisms of cancer development in fibrotic organs.

Keywords

lung cancer --- renal injury --- fibrosis --- crizotinib --- anaplastic lymphoma kinase --- cystic formation --- pulmonary fibrosis --- butylidenephthalide --- SOX2 --- type I collagen --- bleomycin --- YAP --- TAZ --- Hippo pathway --- fibrosis --- cancer --- mechanotransduction --- TGF-? --- Wnt --- uterine fibroid --- leiomyoma --- tumor --- tumor necrosis factor ? --- cytokine --- growth factor --- inflammation --- clinical symptoms --- pathophysiology --- therapy --- hepatocellular carcinoma --- cirrhosis --- regeneration --- inflammation --- cytokines --- genetic instability --- reactive oxygen species --- idiopathic pulmonary fibrosis (IPF) --- lung cancer (LC) --- non-small cell lung cancer (NSCLC) --- acute lung injury --- protein S --- apoptosis --- signal pathway --- Erk1/2 --- lipopolysaccharide --- uterine fibroid --- leiomyoma --- smooth muscle tumor of uncertain malignant potential --- leiomyosarcoma --- myometrium --- immunohistochemistry --- marker --- pathology --- tumor --- diagnosis --- cancer-associated fibroblasts --- tumor microenvironment --- nanoparticles --- breast cancer --- antitumor efficacy --- cirrhosis --- HBV --- HCV --- hepatocellular carcinoma --- idiopathic pulmonary fibrosis --- lung cancer --- pathogenesis --- common pathways --- hepatocellular carcinoma (HCC) --- fibrosis --- cancer-associated fibroblasts (CAFs) --- hepatic stellate cells (HSCs) --- tumor microenvironment --- hepatocellular carcinoma --- non-alcoholic steatohepatitis --- fibrosis --- hepatic stellate cells --- extracellular matrix --- carcinogenesis --- angiogenesis --- cancer-associated fibroblasts --- extracellular matrix --- fibrosis --- heterogeneity --- interstitial fluid pressure --- metabolic reprogramming --- transforming growth factor-? --- tumor stiffness --- GPR40 --- GPR120 --- DHA --- omega-3 fatty acid --- SREBP-1 --- hepatocytes --- EMT --- lncRNA --- metastasis --- miRNA --- SMAD --- TGF-? --- targeted therapy --- tumor microenvironment --- n/a

Diagnosis and Management of Pediatric Diseases

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ISBN: 9783039219667 / 9783039219674 Year: Pages: 146 DOI: 10.3390/books978-3-03921-967-4 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General)
Added to DOAB on : 2020-01-07 09:08:26
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A screenshot of some the most rapidly evolving fields in Neonatology and Pediatrics with articles reviewing some metabolic dysregulations as well as non-oncologic diseases that may occur in infancy, childhood, youth. The illustrative material with original photographs and drawings highlighting some pathogenetic concepts are keystones of this book.

Long-Term Health Effects of the 9/11 Disaster

Authors: --- ---
ISBN: 9783039218127 / 9783039218134 Year: Pages: 298 DOI: 10.3390/books978-3-03921-813-4 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Philosophy
Added to DOAB on : 2019-12-09 11:49:16
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The terrorist attacks on the World Trade Center towers on September 11, 2001, also referred as 9/11, was an iconic event in US history that altered the global and political response to terrorism. The attacks, which involved two planes hitting the twin towers in Lower Manhattan, New York City, resulted in the collapse of the buildings and over 2800 deaths of occupants of the buildings, fire, police and other responders and persons on the street in the vicinity of the collapsing buildings. The destroyed towers and the surrounding buildings have since been replaced but the health effects that resulted from the release of tons of dust, gases and debris as well as the life threat trauma are ongoing, and represent a major health burden among persons directly exposed. Hundreds of scientific publications have documented the physical and mental health effects attributed to the disaster. The current state-of-the-art in understanding the ongoing interactions of physical and mental health, especially PTSD, and the unique mechanisms by which pollutants from the building collapse, have resulted in long term pulmonary dysfunction, course of previously reported conditions, potential emerging conditions (e.g., heart disease and autoimmune diseases), as well as quality of life, functioning and unmet health care needs would be in the purview of this Special Issue on the 9/11 Disaster.

Keywords

counseling --- post-disaster --- psychotherapy --- mental health treatment --- treatment utilization --- World Trade Center --- indoor allergens sensitization --- asthma quality of life --- asthma control --- asthma outcomes --- mini asthma quality of life questionnaire --- asthma morbidity --- WTC-related asthma --- immunoglobulin E --- allergen exposure --- WTC attack --- respiratory symptoms --- lower Manhattan residents --- cleaning practices --- WTC --- fibrotic sarcoid --- injury --- inflammation --- fibrosis --- World Trade Center disaster --- pulmonary fibrosis --- dust --- injury --- physical health --- mental health --- World Trade Center disaster --- Short Form-12 (SF-12) --- HQoL --- 9/11 --- 9/11 disaster --- handgrip strength --- WTC responders --- PTSD --- depression --- aging --- 9/11 impact --- retirement --- chronic disease --- PTSD --- disaster --- income loss --- PTSD symptom change --- PCL score --- longitudinal analysis --- PTSD cluster --- WTC survivors --- 9/11 disaster --- obstructive sleep apnea --- comorbid insomnia --- sleep-related quality of life --- chronic sinusitis --- sleepiness --- WTC responders --- thyroid cancer --- 9/11 disaster --- World Trade Center --- surveillance bias --- sarcoidosis --- World Trade Center (WTC) --- Scadding stage --- lung function --- severe lung disease --- extrathoracic sarcoidosis --- cardiac sarcoidosis --- unmet mental health care needs --- Asian Americans --- World Trade Center attack --- disaster --- mental health conditions --- mental health service use --- health insurance --- social support --- stressful life events --- cognitive reserve --- cognitive decline --- latent class analysis --- disaster epidemiology --- PTSD --- airway physiology --- dust --- environmental health --- forced oscillation --- respiratory function --- small airway disease --- paresthesia --- neuropathic symptoms --- Cox regression --- hazard function --- World Trade Center exposure --- metabolic syndrome --- airway hyperreactivity --- World Trade Center --- disaster mental health --- evidence-based treatment --- mental health service utilization --- quality improvement --- 9/11 --- screening --- thyroid cancer --- biomarkers --- medical imaging --- pulmonary function tests --- lung injury --- occupational exposure --- epidemiological studies --- peripheral neuropathy --- prevalence --- World Trade Center --- rescue/recovery workers --- occupational exposure --- sarcoidosis --- World Trade Center --- 9/11 --- genetics --- firefighters --- FDNY --- 9/11 disaster --- asthma --- trigger(s) --- air pollution --- irritant(s) --- health-related quality of life --- n/a

mTOR in Human Diseases

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ISBN: 9783039210602 / 9783039210619 Year: Pages: 480 DOI: 10.3390/books978-3-03921-061-9 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General)
Added to DOAB on : 2019-06-26 08:44:06
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The mechanistic target of rapamycin (mTOR) is a major signaling intermediary that coordinates favorable environmental conditions with cell growth. Indeed, as part of two functionally distinct protein complexes, named mTORC1 and mTORC2, mTOR regulates a variety of cellular processes, including protein, lipid, and nucleotide synthesis, as well as autophagy. Over the last two decades, major molecular advances have been made in mTOR signaling and have revealed the complexity of the events implicated in mTOR function and regulation. In parallel, the role of mTOR in diverse pathological conditions has also been identified, including in cancer, hamartoma, neurological, and metabolic diseases. Through a series of articles, this book focuses on the role played by mTOR in cellular processes, metabolism in particular, and highlights a panel of human diseases for which mTOR inhibition provides or might provide benefits. It also addresses future studies needed to further characterize the role of mTOR in selected disorders, which will help design novel therapeutic approaches. It is therefore intended for everyone who has an interest in mTOR biology and its application in human pathologies.

Keywords

acute myeloid leukemia --- metabolism --- mTOR --- PI3K --- phosphorylation --- epithelial to mesenchymal transition --- mTOR inhibitor --- pulmonary fibrosis --- transcriptomics --- miRNome --- everolimus --- mTOR --- thyroid cancer --- sodium iodide symporter (NIS)/SLC5A5 --- dopamine receptor --- autophagy --- AKT --- mTOR --- AMPK --- mTOR --- Medulloblastoma --- MBSCs --- mTOR --- T-cell acute lymphoblastic leukemia --- targeted therapy --- combination therapy --- mTOR --- metabolic diseases --- glucose and lipid metabolism --- anesthesia --- neurotoxicity --- synapse --- mTOR --- neurodevelopment --- mTOR --- rapamycin --- autophagy --- protein aggregation --- methamphetamine --- schizophrenia --- tumour cachexia --- mTOR --- signalling --- metabolism --- proteolysis --- lipolysis --- mTOR --- mTORC1 --- mTORC2 --- rapamycin --- rapalogues --- rapalogs --- mTOR inhibitors --- senescence --- ageing --- aging --- cancer --- neurodegeneration --- immunosenescence --- senolytics --- biomarkers --- leukemia --- cell signaling --- metabolism --- apoptosis --- miRNA --- mTOR inhibitors --- mTOR --- tumor microenvironment --- angiogenesis --- immunotherapy --- fluid shear stress --- melatonin --- chloral hydrate --- nocodazole --- MC3T3-E1 cells --- primary cilia --- mTOR complex --- metabolic reprogramming --- cancer --- microenvironment --- nutrient sensor --- oral cavity squamous cell carcinoma (OSCC) --- NVP-BEZ235 --- mTOR --- p70S6K --- mTOR --- advanced biliary tract cancers --- mTOR --- NGS --- illumina --- IonTorrent --- eIFs --- mTOR --- autophagy --- Parkinson’s disease --- mTOR --- PI3K --- cancer --- inhibitor --- therapy --- mTOR --- laminopathies --- lamin A/C --- Emery-Dreifuss muscular dystrophy (EDMD) --- Hutchinson-Gilford progeria syndrome (HGPS) --- autophagy --- cellular signaling --- metabolism --- bone remodeling --- ageing --- mTOR --- fructose --- glucose --- liver --- lipid metabolism --- gluconeogenesis --- Alzheimer’s disease --- autophagy --- mTOR signal pathway --- physical activity --- microRNA --- mTOR --- spermatogenesis --- male fertility --- Sertoli cells --- n/a

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