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Do Both Psychopathology and Creativity Result from a Labile Wake-Sleep-Dream Cycle?

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889453375 Year: Pages: 115 DOI: 10.3389/978-2-88945-337-5 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Psychology
Added to DOAB on : 2018-02-27 16:16:45
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Laypeople think of wake, sleep and dreaming as distinct states of the mind/brain but “in-between”, hybrid states are recognized. For example, day-dreaming or, more scientifically, the default network occurs during wake. Equally, during sleep, lucid dreaming in rapid eye movement (REM) sleep presents as another hybrid state. But hybrid states are usually temporary. This book explores the possibility of an enduring hybrid wake-sleep-dream state, proposing that such a state may engender both creativity and psychopathologies. REM sleep is hyper-associative. Creativity depends on making remote associations. If REM sleep and dreaming begin to suffuse the wake state, enhanced creativity may result. But moderate to severe interpenetration of wake, sleep and dreaming may engender psychopathologies – as the functions of wake, sleep and dreaming are partially eroded.

Fragmentation in Sleep and Mind: Linking Dissociative Symptoms, Sleep, and Memory

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889454488 Year: Pages: 108 DOI: 10.3389/978-2-88945-448-8 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Psychiatry --- Science (General) --- Psychology
Added to DOAB on : 2018-11-16 17:17:57
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Fragmented, dissociated consciousness can characterize the mind in both wake and sleep states. Dissociative symptoms, during sleep, include vivid dreaming, nightmares, and alterations in objective sleep parameters (e.g., lengthening of REM sleep). During waking hours, dissociative symptoms exhibit disparate characteristics encompassing memory problems, excessive daydreaming, absentmindedness, and impairments and discontinuities in perceptions of the self, identity, and the environment. Llewellyn has theorized that a progressive and enduring de-differentiation of wake and dream states of consciousness eventually results in schizophrenia; a lesser degree of de-differentiation may have implications for dissociative symptoms.Against a background of de-differentiation between the dream and wake states, the papers in this volume link consciousness, memory, and mental illness with a special interest for dissociative symptoms.

Mind the gap! Gap junction channels and their importance in pathogenesis

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889192380 Year: Pages: 252 DOI: 10.3389/978-2-88919-238-0 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Medicine (General) --- Therapeutics --- Science (General)
Added to DOAB on : 2015-11-16 15:44:59
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"Cells live together, but die singly", this sentence wrote the German physiologist Theodor Engelmann in 1875 and although he had no particular knowledge of gap junction channels (their structure was discovered around 100 years later) he described their functions very well: gap junction channels are essential for intercellular communication and crucial for the development of tissue and organs. But besides providing an opportunity for cells to communicate gap junction channels might also prevent intercellular communication by channel closure thereby preserving the surrounding healthy tissue in case of cellular necrosis. According to today’s understanding gap junction channels play an important role during embryonic development, during growth, wound healing and cell differentiation and are also involved in the process of learning. In the past decades most intensive research was done not only to unravel the physiological role of gap junction channels but also to extend our knowledge of the contribution of these channels in pathogenesis. A new frontier emerges in the field "pharmacology of gap junctions" with the aim to control growth, differentiation, or electrical coupling via targeting gap junction channels pharmacologically. As we know today disturbances in gap junction synthesis, assembly and cellular distribution may account for various organic disorders from most different medical fields, such as the Charcot-Marie-Tooth neuropathy, epilepsy, Chagas-disease, Naxos-syndrome, congenital cardiac malformations, arrhythmias, cancer and as a very common disease in industrial countries atherosclerosis. Point mutations in gap junction channels have been found to cause hereditary diseases like the congenital deafness or the Charcot-Marie-Tooth neuropathy but the exact molecular mechanisms of gap junction malfunction from most of the mentioned illnesses are not fully understood. Moreover, in the last few years research has expanded on the role and function of connexin hemichannels and on a relatively new field the pannexins. The purpose of this volume is to give a comprehensive overview of the involvement of gap junction channels, hemichannels and pannexins on pathogenesis of inborn and acquired diseases and on emerging pharmacological strategies to target these channels. We welcome our colleagues to contribute their findings on the influence of gap junctions on pathogenesis and to unravel the secrets of intercellular communication. Take the lid off!

Diverse functions of mucosal resident memory T cells

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889195398 Year: Pages: 86 DOI: 10.3389/978-2-88919-539-8 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2016-01-19 14:05:46
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Early studies recognized the unique phenotype and attributes of T cells found in mucosal tissues, such as the intestines, skin, lung and female reproductive tract. This special topic issue will cover many aspects of mucosal-resident T cell biology during infection and disease and is dedicated to Leo Lefrancois, a pioneer in this field who recently passed away. A major proportion of these mucosal T cells are memory T cells, now recognized as a major constituent of memory T cells referred to as tissue-resident memory T cells. Unlike central and effector memory T cell subsets, tissue-resident memory T cells exhibit tissue specificity with minimal systemic migration. Nonetheless, tissue-resident memory T cells share a similar origin and display some overlapping phenotypes with their other memory T cell counterparts. Articles in this issue will describe the different types of memory T cells residing in mucosal tissues, their origins and functions as well as how they vary among discrete mucosal sites. Manuscripts will consider the unique physiological environments and cellular constituents which facilitate tissue residency while preserving tissue function. Additionally, there will be descriptions of the various mechanisms responsible for the migration and segregation of tissue resident memory CD8 T cells from the peripheral T cell pool. Although the mechanisms facilitating the sequestration of tissue-resident memory T cells within a respective tissue has not well characterized, various theories will also be discussed. Lastly, how these T cells contribute to immunity to pathogens, cancer, and autoimmunity and could be modified through vaccination or therapeutic intervention will be described. As mucosal tissues are the major portals of pathogen entry and frequent transformation, the activities and persistence of tissue resident memory T cells is crucial for mediating protection at these sites.

Dendritic Cell and Macrophage Nomenclature and Classification

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199181 Year: Pages: 202 DOI: 10.3389/978-2-88919-918-1 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2016-01-19 14:05:46
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The mononuclear phagocyte system (MPS) comprises dendritic cells (DCs), monocytes and macrophages (MØs) that together play crucial roles in tissue immunity and homeostasis, but also contribute to a broad spectrum of pathologies. They are thus attractive therapeutic targets for immune therapy. However, the distinction between DCs, monocytes and MØ subpopulations has been a matter of controversy and the current nomenclature has been a confounding factor. DCs are remarkably heterogeneous and consist of multiple subsets traditionally defined by their expression of various surface markers. While markers are important to define various populations of the MPS, they do not specifically define the intrinsic nature of a cell population and do not always segregate a bona fide cell type of relative homogeneity. Markers are redundant, or simply define distinct activation states within one subset rather than independent subpopulations. One example are the steady-state CD11b+ DCs which are often not distinguished from monocytes, monocyte-derived cells, and macrophages due to their overlapping phenotype. Lastly, monocyte fate during inflammation results in cells bearing the phenotypic and functional features of both DCs and MØs significantly adding to the confusion. In fact, depending on the context of the study and the focus of the laboratory, a monocyte-derived cell will be either be called "monocyte-derived DCs" or "macrophages". Because the names we give to cells are often associated with a functional connotation, this is much more than simple semantics. The "name" we give to a population fundamentally changes the perception of its biology and can impact on research design and interpretation. Recent evidence in the ontogeny and transcriptional regulation of DCs and MØs, combined with the identification of DC- and MØ-specific markers has dramatically changed our understanding of their interrelationship in the steady state and inflammation. In steady state, DCs are constantly replaced by circulating blood precursors that arise from committed progenitors in the bone marrow. Similarly, some MØ populations are also constantly replaced by circulating blood monocytes. However, others tissue MØs are derived from embryonic precursors, are seeded before birth and maintain themselves in adults by self-renewal. In inflammation, such differentiation pathways are fundamentally changed and unique monocyte-derived inflammatory cells are generated. Current DC, monocyte and MØ nomenclature does not take into account these new developments and as a consequence is quite confusing. We believe that the field is in need of a fresh view on this topic as well as an upfront debate on DC and MØ nomenclature. Our aim is to bring expert junior and senior scientists to revisit this topic in light of these recent developments. This Research Topic will cover all aspects of DC, monocyte and MØ biology including development, transcriptional regulation, functional specializations, in lymphoid and non-lymphoid tissues, and in both human and mouse models. Given the central position of DCs, monocytes and MØs in tissue homeostasis, immunity and disease, this topic should be of interest to a large spectrum of the biomedical community.

The Origin of the Plasma Cell Heterogeneity

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197347 Year: Pages: 80 DOI: 10.3389/978-2-88919-734-7 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2016-04-07 11:22:02
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Plasma cells (PCs) are terminally differentiated B-cells producing large amounts of immunoglobulins (Ig). In humans, most of circulating Ig are produced by bone marrow plasma cells. PCs differentiate from activated naïve or memory B-cells usually activated by specific antigens. It is still controversial whether the regulation of PCs numbers and the “active” in vivo Ig diversity depend or not on non-specific reactivation of B-cells during infections. Depending on the stimulus (T-independent/T-dependent antigen, cytokines, partner cells) and B-cell types (naïve or memory, circulating or germinal center, lymph nodes or spleen, B1 or B2...), both the phenotype and isotype of PCs differ suggesting that PC diversity is either linked to B-cell diversity or to the type of stimulus or to both. Knowledge of the mechanisms supporting PC diversity has important consequences for the management of i) plasma cell neoplasia such as Multiple Myeloma and Waldenström's Macroglobulinemia, ii) vaccine protection against pathogens and iii) auto-immune diseases.

Keywords

Plasma cell --- B-cell --- differentiation --- Cell Cycle --- IL21 --- Autophagy --- B1 --- Autoimmunity --- Myeloma

Mitogen Activated Protein Kinases

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889453399 Year: Pages: 163 DOI: 10.3389/978-2-88945-339-9 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Biology
Added to DOAB on : 2018-02-27 16:16:45
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Mitogen-activated protein kinase (MAPK) pathways are evolutionarily conserved in all eukaryotes and allow cells to respond to changes in the physical and chemical properties of the environment and to produce an appropriate response by altering many cellular functions. MAPKs are among the most intensively studied signal transduction systems. MAPK research is a very dynamic field in which new perspectives are continuously opening to the scientific community. Importantly, many MAPK inhibitors have been developed during the last years and are currently being tested in preclinical and clinical assays for inflammatory diseases and cancer treatment. In this research topic, we have gathered 14 papers covering recent advances in different aspects of the MAPK research area that have provided valuable insight into the spatiotemporal dynamics, the regulation and functions of MAPK pathways, as well as their therapeutic potential. We hope that this Research Topic helps readers to have a better understanding of the progresses that have been made recently in the field of MAPK signalling. A deeper understanding of the these pathways will facilitate the development of innovative therapeutic approaches.

Keywords

MAPK --- p38 --- ERK --- JNK --- MSK --- kinase --- scaffold --- cancer --- inflammation --- cell differentiation

Assessing Prenatal and Neonatal Gonadal Steroid Exposure for Studies of Human Development: Methodological and Theoretical Challenges

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196074 Year: Pages: 80 DOI: 10.3389/978-2-88919-607-4 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Internal medicine
Added to DOAB on : 2016-08-16 10:34:25
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There is extensive evidence from animal models that gonadal steroids, produced in fetal and neonatal life, act on the developing organism to produce sex differences far beyond the reproductive system. That early gonadal steroid exposure also plays an important role in human development is supported by studies of individuals with disorders of sex determination and differentiation. It is much less clear whether normal variation in gonadal steroid exposure predicts sexually dimorphic health outcomes or within-sex variation. This is largely due to challenges related to the assessment of gonadal steroid exposure in the developing fetus and neonate. Regarding the prenatal period, serial measurements of serum hormone levels in the fetus, for use in studies of later development, are not possible for ethical reasons. Researchers have measured hormones in maternal blood, umbilical cord blood, and amniotic fluid; used putative anthropometric indices such as the relative lengths of the 2nd and 4th digits (2D:4D); evaluated common variants in genes related to hormone production, transport, and metabolism; and examined development in opposite sex twins and the offspring of mothers with hyperandrogeny. Each of these approaches has particular strengths and notable weaknesses. Regarding the neonatal period, serial measurements in serum are often impractical for studies of typical development. Salivary hormone assays, frequently used in studies of older children and adults, have not been extensively investigated in neonates. The most appropriate timing for testing is also open to debate. Early work suggested that testosterone levels in males begin to rise after the first postnatal week, peak around the 3rd to 4th months of life, and then drop back to very low levels by 1 year. However a more recent study of 138 infants did not demonstrate this pattern. Testosterone was highest on the day of birth and gradually dropped over the first 6 months. Even less is known about patterns of early estrogen exposure, though highly sensitive bioassays indicated that sex differences are present in early childhood. In addition, the design and interpretation of studies may be impacted by widespread acceptance of conceptual frameworks that are not well-supported empirically. For example, many researchers presume that the free hormone hypothesis, which states that unbound hormone is more readily diffusible into tissues and thus a better measure of actual exposure, is true. However this hypothesis has been challenged on multiple grounds. A second example: it is generally accepted that masculinization of the human brain is primarily mediated by the androgen receptor (in contrast to rodents where the estrogen receptor plays a major role), in part because chromosomal males with complete androgen insensitivity generally espouse a female gender identity. However this is not always the case, and other sexually dimorphic outcomes have not been carefully assessed in CAIS. The aim of this research topic is to gather together experimental and review papers which address the diverse challenges in assessing prenatal and neonatal gonadal steroid exposure for studies of human development with the expectation that this will allow more critical appraisal of existing studies, identify critical research gaps, and improve the design of future studies.

Mobile Genetic Elements in Cellular Differentiation, Genome Stability, and Cancer

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889453894 Year: Pages: 123 DOI: 10.3389/978-2-88945-389-4 Language: English
Publisher: Frontiers Media SA
Subject: Biology --- Science (General) --- Chemistry (General)
Added to DOAB on : 2018-11-22 11:50:10
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The human genome, as with the genome of most organisms, is comprised of various types of mobile genetic element derived repeats. Mobile genetic elements that mobilize by an RNA intermediate, include both autonomous and non-autonomous retrotransposons, and mobilize by a “copy and paste” mechanism that relies of the presence of a functional reverse transcriptase activity. The extent to which these different types of elements are actively mobilizing varies among organisms, as revealed with the advent of Next Generation DNA sequencing (NGS).To understand the normal and aberrant mechanisms that impact the mobility of these elements requires a more extensive understanding of how these elements interact with molecular pathways of the cell, including DNA repair, recombination and chromatin. In addition, epigenetic based-mechanisms can also influence the mobility of these elements, likely by transcriptional activation or repression in certain cell types. Studies regarding how mobile genetic elements interface and evolve with these pathways will rely on genomic studies from various model organisms. In addition, the mechanistic details of how these elements are regulated will continue to be elucidated with the use of genetic, biochemical, molecular, cellular, and bioinformatic approaches. Remarkably, the current understanding regarding the biology of these elements in the human genome, suggests these elements may impact developmental biology, including cellular differentiation, neuronal development, and immune function. Thus, aberrant changes in these molecular pathways may also impact disease, including neuronal degeneration, autoimmunity, and cancer.

Physiology and Pathophysiology of the Extracellular Calcium-Sensing Receptor

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889455126 Year: Pages: 189 DOI: 10.3389/978-2-88945-512-6 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Physiology
Added to DOAB on : 2019-01-23 14:53:42
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Calcium is vital for human physiology; it mediates multiple signaling cascades, critical for cell survival, differentiation, or death both as first and as second messenger. The role of calcium as first messenger is mediated by the G-protein coupled receptor, the extracellular calcium-sensing receptor (CaSR). The CaSR is a multifaceted molecule that senses changes in the concentration of a wide variety of environmental factors including di- and trivalent cations, amino acids, polyamines, and pH. In calcitropic tissues with obvious roles in calcium homeostasis such as parathyroid, kidney, and bone it regulates circulating calcium concentrations. The germline mutations of the CaSR cause parathyroid disorders demonstrating the importance of the CaSR for the maintenance of serum calcium homeostasis. The CaSR has an important role also in a range of non-calcitropic tissues, such as the intestine, lungs, central and peripheral nervous system, breast, skin and reproductive system, where it regulates molecular and cellular processes such as gene expression, proliferation, differentiation and apoptosis; as well as regulating hormone secretion and lactation.This Research Topic is an overview of the CaSR and its molecular signaling properties together with the various organ systems where it plays an important role. The articles highlight the current knowledge regarding many aspects of the calcitropic and non-calcitropic physiology and pathophysiology of the CaSR.

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