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A finely tuned regulation of gene expression is essential for shaping the nervous system and for maintaining its homeostasis throughout life. Disruptions in gene regulation can impact brain development and physiology in ways that contribute to diverse pathologies. The master orchestrators of gene activity in the nucleus are transcription factors, proteins that recognize and bind to specific DNA motifs in regulatory regions and drive changes in gene expression. Transcription factors act with the help of other co-factor proteins, including components of the Mediator complex, histone modifying enzymes, chromatin modelers, and DNA methylases. In addition, transcription factor activity in the nervous system can be modulated by extracellular signals, including growth factors, hormones, neuropeptides and neurotransmitters that activate specific receptors and intracellular transduction pathways. An in-depth understanding of the mechanisms of transcription regulation is needed in order to better describe how each element, from genes to cells, defines and maintains identities and functionalities in the healthy and diseased brain. This Research Topic is oriented to developing an integrative view about transcription regulation within the nervous system, focusing on developmental and homeostatic processes, dysregulation in functionality and expression levels and consequent associated pathologies such as neurodevelopmental disorders, brain tumors, and neurodegenerative diseases. Transcription regulation investigations will specifically focus on transcription factors that belong to the bHLH (e.g. NeuroD), homeobox (e.g. Islet, Pax, Rax, and Lhx) and CREB families, and on their roles over defined nervous system areas: cerebral cortex, thalamic and hypothalamic areas, interacting with the developing brain.
The functional anatomy of organisms is maintained by the coordination of different systems, that often rely on particular interactions between specialized cells and between macromolecules. The immune system works with the circulatory and the lymphatic systems to protect most of the organs. However, some organs are considered immune privileged due to the presence of highly selective and regulated barriers, such as the blood-brain barrier (BBB) within the brain. The BBB controls periphery-brain molecule exchange and prevents immune effector cells from entering the homeostatic brain. BBB-associated elements, such as endothelial cells, pericytes, astrocytes, and microglia, potentially can function as antigen-presenting cells (APC). Pathological scenarios that induce dysfunction of the BBB and its associated cells may lead to the infiltration of lymphocytes crossing over from the blood to brain. Similarly, traumas can also enable B and T lymphocytes to pass bidirectionally between the CNS and the periphery, via the meningeal lymphatic vessels which drain into the cervical lymph nodes. Research in animals and in humans has revealed that B and T cells are involved in the progression of neurological diseases. It has been showed that under particular conditions, T cells establish themselves and become resident in the brain (T RM cells), from where they can either exert beneficial or detrimental effects on brain function. Amazing efforts have been made to further comprehend interactions between brain-specific cells and peripheral immune cells, and especially their roles and impact on the onset, progression, and eventual resolution of diverse brain pathologies.
The CA3 hippocampal region receives information from the entorhinal cortex either directly from the perforant path or indirectly from the dentate gyrus via the mossy fibers (MFs). According to their specific targets (principal/mossy cells or interneurons), MFs terminate with large boutons or small filopodial extensions, respectively. MF-CA3 synapses are characterized by a low probability of release and pronounced frequency-dependent facilitation. In addition MF terminals are endowed with mGluRs that regulate their own release. We will describe the intrinsic membrane properties of pyramidal cells, which can sometimes fire in bursts, together with the geometry of their dendritic arborization. The single layer of pyramidal cells is quite distinct from the six-layered neocortical arrangement. The resulting aligned dendrites provides the substrate for laminated excitatory inputs. They also underlie a precise, diversity of inhibitory control which we will also describe in detail. The CA3 region has an especially rich internal connectivity, with recurrent excitatory and inhibitory loops. In recent years both in vivo and in vitro studies have allowed to better understand functional properties of the CA3 auto-associative network and its role in information processing. This circuit is implicated in encoding spatial representations and episodic memories. It generates physiological population synchronies, including gamma, theta and sharp-waves that are presumed to associate firing in selected assemblies of cells in different behavioral conditions. The CA3 region is susceptible to neurodegeneration during aging and after stresses such as infection or injury. Loss of some CA3 neurones has striking effects on mossy fiber inputs and can facilitate the generation of pathologic synchrony within the CA3 micro-circuit. The aim of this special topic is to bring together experts on the cellular and molecular mechanisms regulating the wiring properties of the CA3 hippocampal microcircuit in both physiological and pathological conditions, synaptic plasticity, behavior and cognition.We will particularly emphasize the dual glutamatergic and GABAergic phenotype of MF-CA3 synapses at early developmental stages and the steps that regulate the integration of newly generated neurons into the adult dentate gyrus-CA3 circuit.
Angiogenesis, the development of new blood vessels from the existing vasculature, is essential for physiological growth and over 18,000 research articles have been published describing the role of angiogenesis in over 70 different diseases, including cancer, diabetic retinopathy, rheumatoid arthritis and psoriasis. One of the most important technical challenges in such studies has been finding suitable methods for assessing the effects of regulators of eh angiogenic response. While increasing numbers of angiogenesis assays are being described both in vitro and in vivo, it is often still necessary to use a combination of assays to identify the cellular and molecular events in angiogenesis and the full range of effects of a given test protein. Although the endothelial cell - its migration, proliferation, differentiation and structural rearrangement - is central to the angiogenic process, it is not the only cell type involved. the supporting cells, the extracellular matrix and the circulating blood with its cellular and humoral components also contribute. In this book, experts in the use of a diverse range of assays outline key components of these and give a critical appraisal of their strengths and weaknesses. Examples include assays for the proliferation, migration and differentiation of endothelial cells in vitro, vessel outgrowth from organ cultures, assessment of endothelial and mural cell interactions, and such in vivo assays as the chick chorioallantoic membrane, zebrafish, corneal, chamber and tumour angiogenesis models. These are followed by a critical analysis of the biological end-points currently being used in clinical trials to assess the clinical efficacy of anti-angiogenic drugs, which leads into a discussion of the direction future studies should take. This valuable book is of interest to research scientists currently working on angiogenesis in both the academic community and in the biotechnology and pharmaceutical industries. Relevant disciplines include cell and molecular biology, oncology, cardiovascular research, biotechnology, pharmacology, pathology and physiology.
Recent studies have indicated that epigenetic processes may play a major role in both cellular and organismal aging. These epigenetic processes include not only DNA methylation and histone modifications, but also extend to many other epigenetic mediators such as the polycomb group proteins, chromosomal position effects, and noncoding RNA. The topics of this book range from fundamental changes in DNA methylation in aging to the most recent research on intervention into epigenetic modifications to modulate the aging process. The major topics of epigenetics and aging covered in this book are: 1) DNA methylation and histone modifications in aging; 2) Other epigenetic processes and aging; 3) Impact of epigenetics on aging; 4) Epigenetics of age-related diseases; 5) Epigenetic interventions and aging: and 6) Future directions in epigenetic aging research. The most studied of epigenetic processes, DNA methylation, has been associated with cellular aging and aging of organisms for many years. It is now apparent that both global and gene-specific alterations occur not only in DNA methylation during aging, but also in several histone alterations. Many epigenetic alterations can have an impact on aging processes such as stem cell aging, control of telomerase, modifications of telomeres, and epigenetic drift can impact the aging process as evident in the recent studies of aging monozygotic twins. Numerous age-related diseases are affected by epigenetic mechanisms. For example, recent studies have shown that DNA methylation is altered in Alzheimer’s disease and autoimmunity. Other prevalent diseases that have been associated with age-related epigenetic changes include cancer and diabetes. Paternal age and epigenetic changes appear to have an effect on schizophrenia and epigenetic silencing has been associated with several of the progeroid syndromes of premature aging. Moreover, the impact of dietary or drug intervention into epigenetic processes as they affect normal aging or age-related diseases is becoming increasingly feasible.
This fourth edition of the best-selling textbook, Human Genetics and Genomics, clearly explains the key principles needed by medical and health sciences students, from the basis of molecular genetics, to clinical applications used in the treatment of both rare and common conditions. A newly expanded Part 1, Basic Principles of Human Genetics, focuses on introducing the reader to key concepts such as Mendelian principles, DNA replication and gene expression. Part 2, Genetics and Genomics in Medical Practice, uses case scenarios to help you engage with current genetic practice. Now featuring full-color diagrams, Human Genetics and Genomics has been rigorously updated to reflect today’s genetics teaching, and includes updated discussion of genetic risk assessment, “single gene” disorders and therapeutics. Key learning features include: Clinical snapshots to help relate science to practice 'Hot topics' boxes that focus on the latest developments in testing, assessment and treatment 'Ethical issues' boxes to prompt further thought and discussion on the implications of genetic developments 'Sources of information' boxes to assist with the practicalities of clinical research and information provision Self-assessment review questions in each chapter Accompanied by the Wiley E-Text digital edition (included in the price of the book), Human Genetics and Genomics is also fully supported by a suite of online resources at www.korfgenetics.com, including: Factsheets on 100 genetic disorders, ideal for study and exam preparation Interactive Multiple Choice Questions (MCQs) with feedback on all answers Links to online resources for further study Figures from the book available as PowerPoint slides, ideal for teaching purposes The perfect companion to the genetics component of both problem-based learning and integrated medical courses, Human Genetics and Genomics presents the ideal balance between the bio-molecular basis of genetics and clinical cases, and provides an invaluable overview for anyone wishing to engage with this fast-moving discipline.
This volume connects current ideas and concepts about sleep functions and circadian rhythms with the search for novel target-selective sleep-wake therapeutics. To do so, it provides a timely, state-of-the-art overview of sleep-wake mechanisms in health and disease, ongoing developments in drug discovery, and their prospects for the clinical treatment of sleep-disordered patients. It particularly focuses on the concept that sleep and wakefulness mutually affect each other, and the future therapeutic interventions with either sleep- or wake-promoting agents that are expected to not only improve the quality of sleep but also the waking behavior, cognition, mood and other sleep-associated physiological functions. The chapter 'Sleep Physiology, Circadian Rhythms, Waking Performance and the Development of Sleep-Wake Therapeutics' available open access under a CC BY 4.0 license at link.springer.com
This volume examines in detail the role of chronic inflammatory processes in the development of several types of cancer. Leading experts describe the latest results of molecular and cellular research on infection, cancer-related inflammation and tumorigenesis. Further, the clinical significance of these findings in preventing cancer progression and approaches to treating the diseases are discussed. Individual chapters cover cancer of the lung, colon, breast, brain, head and neck, pancreas, prostate, bladder, kidney, liver, cervix and skin as well as gastric cancer, sarcoma, lymphoma, leukemia and multiple myeloma.