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The Natriuretic Hormones

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197095 Year: Pages: 76 DOI: 10.3389/978-2-88919-709-5 Language: English
Publisher: Frontiers Media SA
Subject: Internal medicine --- Medicine (General)
Added to DOAB on : 2016-04-07 11:22:02
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The title follows from the original demonstration by Dr. Hugh de Wardener in 1961 that a humoral agent is produced after extracellular volume expansion which results in a vigorous diuresis and natriuresis. Thus the name of "natriuretic hormone" was coined. In the years that followed several investigators pursued the search for the hormone. What resulted, however, was the discovery of several hormones with different characteristics, all of which were natriuretic. Initially it was found that the hormone was similar in action to ouabain or digoxin, hence the appelation of ouabain-like or digoxin-like. The hormone was found to be an inhibitor of Na-K-ATPase, which would fit with it being a cardiotonic steroid. On the other hand, neither ouabain or digoxin migrated on Sephadex gel filtration in the same locus as the hormone. Other investigators claim to have identified the hormone-initially as a vanadium-diascorbate, later as bufadienolides such as marinobufagenin, yet later as a macrocylic derivative of inorganic carbon suboxide with a molecular weight of 408 Da. Some support for the latter finding was derived from an earlier report that a semi-purified Sephadex-derived compound was found to have a molecular weight of about 12,000 Da but the active compound, when split from its carrier protein, had a molecular weight of exactly 408 Da. This compound had not been further identified. As further development was the demonstration by Bricker and colleagues that a natriuretic substance could be purified from uremic urine. This turned out to be a xathurenic acid derivative. Meanwhile the focus began to turn to natriuretic peptides derived from heart (ANF and BNP). These peptides have a shorter duration of action than the cardiotonic steroid-like hormone and ANF has proved to be most useful as a measure of heart failure. It should also be stressed that marinobufagenin, like ANF, is elevated in congestive heart failure, whereas the steroid-like hormone is depressed or absent in this state. This review will attempt to describe and contrast the properties of each of the proposed natriuretic hormones, including their locus on Sephadex separation, potency, duration of action, chemical structure (if known), behavior in hypertension, renal failure, heart failure, and brain disease. As most recent work has focussed on marinobufagenin, this hormone will be brought up to date by investigators in the field.

Essential Pathways and Circuits of Autism Pathogenesis

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199051 Year: Pages: 181 DOI: 10.3389/978-2-88919-905-1 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology --- Genetics
Added to DOAB on : 2016-01-19 14:05:46
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The Centers for Disease Control and Prevention estimate that 1 in 68 children in the United states is afflicted with autism spectrum disorders (ASD), yet at this time, there is no cure for the disease. Autism is characterized by delays in the development of many basic skills, most notably the ability to socialize and adapt to novelty. The condition is typically identified in children around 3 years of age, however the high heritability of autism suggests that the disease process begins at conception. The identification of over 500 ASD risk genes, has enabled the molecular genetic dissection of the pathogenesis of the disease in model organisms such as mice. Despite the genetic heterogeneity of ASD etiology, converging evidence suggests that these disparate genetic lesions may result in the disruption of a limited number of key biochemical pathways or circuits. Classification of patients into groups by pathogenic rather than etiological categories, will likely aid future therapeutic development and clinical trials. In this set of papers, we explore the existing evidence supporting this view. Specifically, we focus on biochemical cascades such as mTOR and ERK signaling, the mRNA network bound by FMRP and UBE3A, dorsal and ventral striatal circuits, cerebellar circuits, hypothalamic projections, as well as prefrontal and anterior cingulate cortical circuits. Special attention will be given to studies that demonstrate the necessity and/or sufficiency of genetic disruptions (e.g. by molecular deletion and/or replacement) in these pathways and circuits for producing characteristic behavioral features of autism. Necessarily these papers will be heavily weighted towards basic mechanisms elucidated in animal models, but may also include investigations in patients.

Neuroendocrine mechanisms that connect feeding behavior and stress

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889195077 Year: Pages: 189 DOI: 10.3389/978-2-88919-507-7 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2015-12-03 13:02:24
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Research during the past decade highlights the strong link between appetitive feeding behavior, reward and motivation. Interestingly, stress levels can affect feeding behavior by manipulating hypothalamic circuits and brain dopaminergic reward pathways. Indeed, animals and people will increase or decrease their feeding responses when stressed. In many cases acute stress leads to a decrease in food intake, yet chronic social stressors are associated to increases in caloric intake and adiposity. Interestingly, mood disorders and the treatments used to manage these disorders are also associated with changes in appetite and body weight. These data suggest a strong interaction between the systems that regulate feeding and metabolism and those that regulate mood. This Research Topic aims to illustrate how hormonal mechanisms regulate the nexus between feeding behavior and stress. It focuses on the hormonal regulation of hypothalamic circuits and/or brain dopaminergic systems, as the potential sites controlling the converging pathways between feeding behavior and stress.

Neural Circuits: Japan

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889194377 Year: Pages: 220 DOI: 10.3389/978-2-88919-437-7 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-01-19 14:05:46
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This Frontiers Research Topic on ‘Neural Circuits: Japan’ explores the diversity of neural circuit research occurring across Japan by innovative researchers using cutting-edge approaches. This issue has brought together papers revealing the development, structure, and physiology of neuronal circuits involved in sensory perception, sleep and wakefulness, behavioral selection, and motor command generation in a range of species from the nematode to the primate. Like the USA and Europe, Japan is now making a strong effort to elucidate neural circuit function in diverse organisms by taking advantages of optogenetics and innovative approaches for gene manipulation, traditional physiological and anatomical approaches, and neural pathway-selective inactivation techniques that have recently been developed in Japan.

AMP-Activated Protein Kinase Signalling

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ISBN: 9783038976622 Year: Pages: 452 DOI: 10.3390/books978-3-03897-663-9 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Science (General) --- Biology
Added to DOAB on : 2019-03-21 14:08:22
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Starting from a kinase of interest, AMP-activated protein kinase (AMPK) has gone far beyond an average biomolecule. Being expressed in all mammalian cell types and probably having a counterpart in every eukaryotic cell, AMPK has attracted interest in virtually all areas of biological research. Structural and biophysical insights have greatly contributed to a molecular understanding of this kinase. From good old protein biochemistry to modern approaches, such as systems biology and advanced microscopy, all disciplines have provided important information. Thus, multiple links to cellular events and subcellular localizations have been established. Moreover, the crucial involvement of AMPK in human health and disease has been evidenced. AMPK accordingly has moved from an interesting enzyme to a pharmacological target. However, despite our extensive current knowledge about AMPK, the growing community is busier than ever. This book provides a snapshot of recent and current AMPK research with an emphasis on work providing molecular insight, including but not limited to novel physiological and pathological functions, or regulatory mechanisms. Up-to-date reviews and research articles are included.

Keywords

exercise --- glucose uptake --- AMP-activated protein kinase --- TBC1D4 --- AS160 --- AMP-activated protein kinase --- developmental origins of health and disease (DOHaD) --- hypertension --- kidney disease --- nutrient-sensing signals --- oxidative stress --- renin-angiotensin system --- AMPK --- autophagy --- co-expression --- microarrays --- 3T3-L1 --- adipocyte --- differentiation --- AMPK --- tight junctions --- epithelial cells --- ZO-1 --- par complex --- MDCK --- nectin-afadin --- adherent junctions --- TAK1 --- AMPK --- phosphorylation --- AMPK kinase --- endothelial nitric-oxide synthase --- vasodilation --- phenylephrine --- vasoconstriction --- endothelial cells --- ionomycin --- AMPK --- liver --- lipid metabolism --- fatty acid oxidation --- indirect calorimetry --- atrophy --- regrowth --- sirtuin 1 (SIRT1) --- peroxisome proliferator-activated receptor gamma coactivator 1-? (PGC1?) --- heat shock protein --- fiber-type --- AMPK --- monocytes --- macrophages --- differentiation --- autophagy --- AML --- MDS --- CML --- CMML --- pregnancy --- catechol-O-methyltransferase --- 2-methoxyestradiol --- preeclampsia --- gestational diabetes mellitus --- AMPK --- IL-1? --- NLRP3 --- nutrition --- dietary fatty acids --- metabolic-inflammation --- nutrigenomics --- AMPK --- LKB1 --- autophagy --- proteasome --- hypertrophy --- atrophy --- skeletal muscle --- AICAR --- mTOR --- protein synthesis --- AMPK --- epigenetics --- chromatin remodeling --- histone modification --- DNA methylation --- medulloblastoma --- sonic hedgehog --- AMPK --- AMP-activated protein kinase (AMPK) --- spermatozoa --- motility --- mitochondria --- membranes --- signaling --- stress --- assisted reproduction techniques --- AMP-activated protein kinase --- epigenetics --- protein acetylation --- KATs --- HDACs --- acetyl-CoA --- NAD+ --- AMP-activated protein kinase --- glycogen --- exercise --- metabolism --- cellular energy sensing --- energy utilization --- liver --- skeletal muscle --- metabolic disease --- glycogen storage disease --- resveratrol --- AMPK --- hepatocyte --- liver --- steatosis --- transporter --- carrier --- pump --- membrane --- energy deficiency --- AMPK --- infection --- mycobacteria --- host defense --- energy metabolism --- AMPK --- activation loop --- AID --- ?-linker --- ?-linker --- CBS --- LKB1 --- CaMKK2 --- ?RIM --- hypothalamus --- adenosine monophosphate-activated protein kinase --- adipose tissue --- food intake --- adaptive thermogenesis --- beiging --- AMPK --- HDAC4/5 --- p70S6K --- MyHC I(?), motor endplate remodeling --- soleus muscle --- mechanical unloading --- hindlimb suspension --- AMPK --- synaptic activation --- PKA --- CREB --- soluble Adenylyl cyclase --- Immediate early genes --- transcription --- AMPK --- autophagy --- metabolism --- mTOR --- ULK --- AMP-activated protein kinase --- protein kinase B --- Akt --- insulin signalling --- A769662 --- endothelial function --- n/a

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