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  • 1
    Online-Ressource
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    Epigenetic pathways in PTSD : how traumatic experiences leave their signature on the genome (2015)
    Switzerland :Frontiers Media SA,
    Details
    UID:
    almafu_9958088820802883
    Umfang: 1 online resource (158 pages) : , illustrations, charts.
    ISBN: 9782889193080 (ebook)
    Serie: Frontiers Research Topics
    Inhalt: Epidemiological evidence supports a role for gene-environmental interactions in post-traumatic stress disorder (PTSD). Because environmental exposure to trauma is an etiological factor necessary for the development of PTSD, understanding the molecular mechanisms by which genes respond to traumatic stress may provide insight into the development and life-long persistence of PTSD symptoms. Emerging evidence suggests that DNA methylation, histone modifications, noncoding RNA regulation, and alternative splicing of mRNA provide an epigenetic means by which chronic stress and traumatic experiences alter gene expression to produce long-term changes in neuroanatomy, physiology and behavior. This research topic will focus on epigenetic components of PTSD, and highlight translational research including common measures and outcomes of stress and trauma found in animal, civilian and military research. We will also consider observational and epidemiologic studies that support epigenetic transmission of stress-related phenotypes. We aim to provide a forum for experts in the field to present novel research findings, methodology, opinions, hypotheses and critical reviews that address how traumatic stress interacts with the genome.
    Anmerkung: Bibliographic Level Mode of Issuance: Monograph , English
    Sprache: Englisch
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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    HU Berlin
    FU Berlin
    Charité
  • 2
    Online-Ressource
    Online-Ressource
    Evolution of NK-mediated target recognition under the pressure of physiologic or pathologic stimuli / (2015)
    Switzerland :Frontiers Media SA,
    Details
    UID:
    almafu_9958116395902883
    Umfang: 1 online resource (190 pages) : , illustrations.
    ISBN: 9782889193080 (ebook)
    Serie: Frontiers Research Topics
    Anmerkung: Bibliographic Level Mode of Issuance: Monograph , English
    Sprache: Englisch
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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    HU Berlin
    FU Berlin
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  • 3
    Online-Ressource
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    Immune system modeling and analysis / (2015)
    [Lausanne, Switzerland] :Frontiers Media SA,
    Details
    UID:
    almafu_9958106873202883
    Umfang: 1 online resource (401 pages): , illustrations.
    ISBN: 9782889193080 (ebook)
    Serie: Frontiers Research Topics
    Inhalt: This Research Topic is cross-listed in the Specialty section T Cell biology in Frontiers in Immunology. All submissions on T Cell biology should be submitted through the link: Specialty section T cell Biology in Frontiers in ImmunologyThe rapid development of new methods for immunological data collection – from multicolor flow cytometry, through single-cell imaging, to deep sequencing – presents us now, for the first time, with the ability to analyze and compare large amounts of immunological data in health, aging and disease. The exponential growth of these datasets, however, challenges the theoretical immunology community to develop methods for data organization and analysis. Furthermore, the need to test hypotheses regarding immune function, and generate predictions regarding the outcomes of medical interventions, necessitates the development of mathematical and computational models covering processes on multiple scales, from the genetic and molecular to the cellular and system scales.The last few decades have seen the development of methods for presentation and analysis of clonal repertoires (those of T and B lymphocytes) and phenotypic (surface-marker based) repertoires of all lymphocyte types, and for modeling the intricate network of molecular and cellular interactions within the immune systems. The proposed research topic will provide a comprehensive, online, open access snapshot of the current state of the art on immune system modeling and analysis.The Research Topic will be organized according to the following themes; authors will be asked to identify the most suitable theme for their paper:• Immune cell activation and signaling• Immune cell population dynamics and turnover• Lymphocyte repertoires• Lymphocyte migration and immune tissue organization• Immune responses to pathogens• Immunological diseases• Immune system aging
    Sprache: Englisch
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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    HU Berlin
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  • 4
    Online-Ressource
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    Brain reward and stress systems in addiction / : topic editors: Nicholas W. Gilpin and Remi Martin-Fardon. (2015)
    France :Frontiers Media SA,
    Details
    UID:
    almafu_9958116400502883
    Umfang: 1 online resource (184 pages) : , illustrations; digital, PDF file(s).
    ISBN: 9782889193080
    Serie: Frontiers Research Topics
    Inhalt: Addiction to drugs and alcohol is a dynamic and multi-faceted disease process in humans, with devastating health and financial consequences for the individual and society-at-large. In humans, drug and alcohol use disorders (i.e., abuse and dependence) are defined by clusters of behavioural symptoms that can be modelled to various degrees in animals. Hallmark behavioural symptoms associated with drug and alcohol dependence are compulsive drug use, loss of control during episodes of drug use, the emergence of a negative emotional state in the absence of the drug, and chronic relapse vulnerability during drug abstinence. The transition to drug dependence is defined by neuroadaptations in brain circuits that, in the absence of drugs, mediate a variety of critical behavioural and physiological processes including natural reward, positive and negative emotional states, nociception, and feeding. Chronic drug exposure during the transition to dependence spurs (1) within-systems changes in neural circuits that contribute to the acute rewarding effects of the drug and (2) recruitment of brain stress systems (neuroendocrine and extra-hypothalamic).There are substantial genetic contributions to the propensity to use and abuse drugs, and drug abuse is highly co-morbid with various other psychiatric conditions (e.g., anxiety disorders, major depressive disorder) that may precede or follow the development of drug use problems. Across drugs of abuse, there are overlapping and dissociable aspects of the behavioural and neural changes that define the transition to dependence. Even within a single drug, people abuse drugs for a variety of reasons. The picture is further complicated by the fact that humans often abuse more than one drug concurrently. Even in the face of these challenges, pre-clinical and clinical research is making exponential gains into understanding the neurobiology of drug addiction. With the advent of new technologies and their combination with traditional approaches, the field is able to ask and answer addiction-related research questions in increasingly sophisticated ways. Here, we hope to assemble a collection of articles that provide an up-to-the-moment snapshot of the prevailing empirical, theoretical and technical directions in the addiction research field. We encourage submissions from all investigators working to understand the neurobiology of addiction, especially as it pertains to reward and stress pathways in the brain.
    Anmerkung: Bibliographic Level Mode of Issuance: Monograph , English
    Sprache: Englisch
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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    Online-Ressource
    HU Berlin
    FU Berlin
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  • 5
    Online-Ressource
    Online-Ressource
    Molecular mechanisms of cellular stress responses in cancer and their therapeutic implications / (2015)
    France :Frontiers Media SA,
    Details
    UID:
    almafu_9958126325802883
    Umfang: 1 online resource (159 pages) : , illustrations; digital, PDF file(s).
    ISBN: 9782889193080
    Serie: Frontiers Research Topics
    Inhalt: In response to stress, cells can activate a myriad of signalling pathways to bring about a specific cellular outcome, including cell cycle arrest, DNA repair, senescence and apoptosis. This response is pivotal for tumour suppression as all of these outcomes result in restriction of the growth and/or elimination of damaged and pre-malignant cells. Thus, a large number of anti-cancer agents target specific components of stress response signalling pathways with the aim of causing tumour regression by stimulating cell death. However, the efficacy of these agents is often impaired due to mutations in genes that are involved in these stress-responsive signalling pathways and instead the oncogenic potential of a cell is increased leading to the initiation and/or progression of tumourigenesis. Moreover, these genetic defects can increase or contribute to resistance to chemotherapeutic agents and/or radiotherapy. Modulating the outcome of cellular stress responses towards cell death in tumour cells without affecting surrounding normal cells is thus one of the ultimate aims in the development of new cancer therapeutics. To achieve this aim, a detailed understanding of cellular stress response pathways and their aberrations in cancer is required. This Research topic aims to reflect the broadness and complexity of this important area of cancer research. We encourage original studies, perspectives and review articles that relate to any aspect of cellular stress responses, from both a molecular and clinical perspective. Topics may include signal transduction pathways and genes/proteins regulating them; different stress stimuli (DNA damage, viruses, metabolic stress, hormones and others); cell cycle checkpoints, DNA repair, autophagy, apoptosis and other forms of cell death; mechanisms of resistance against cytotoxic drugs; novel strategies and drugs that interfere with cellular stress responses; and methods to study cellular stress responses. Articles that focus on a specific type of cancer with known characteristics related to cellular stress responses, for example melanoma or therapy-related cancers are also welcome.
    Anmerkung: Bibliographic Level Mode of Issuance: Monograph , English
    Sprache: Englisch
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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    HU Berlin
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  • 6
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    Experimental models of early exposure to alcohol : a way to unravel the neurobiology of mental retardation (2015)
    France :Frontiers Media SA,
    Details
    UID:
    almafu_9958074815102883
    Umfang: 1 online resource (105 pages) : , illustrations; digital, PDF file(s).
    ISBN: 9782889193080
    Inhalt: Excessive alcohol drinking represents a major social and public health problem for several countries. Alcohol abuse during pregnancy leads to a complex clinical disorder referred to as fetal alcohol spectrum disorder (FASD), chiefly characterized by mental retardation (MR). The effects of early exposure to ethanol can be reproduced in laboratory animals and this helped to answer several key questions concerning the human pathology. The interest of experimental models of FASD is twofold. Firstly, they increase our knowledge about the dose and modality of alcohol consumption able to induce damaging effects on the developing brain (see Valenzuela et al., TINS 35: 284-292, 2012). Therefore, laboratory research can help to refine health policy strategies aimed at the prevention of FASD. Second, experimental models of FASD can provide useful hints to elucidate the basic mechanisms leading to MR. In fact, experimental exposure to alcohol can be carried out during discrete, often very restricted time windows. As a consequence, FASD models, though depending on the multifaceted interference of alcohol with several molecular pathways, can nonetheless provide valuable information about which specific developmental periods and brain areas are critically involved in the genesis of MR. On the contrary, experimental models of genetically determined MR are ideally suited to study the involvement of single molecules (e.g, the fragile X mental retardation protein).Putting together the rich ensemble of data obtained through the various experimental paradigms of alcohol exposure, as well as those deriving from other genetic and non-genetic models, one can figure out to what extent different types of MR share common pathogenetic mechanisms, regardless of whether the aetiological factors intervene during different phases of neural development, or affect different brain structures. The present Research Topic is aimed at establishing the state of the art of the current research on experimental FASD, focusing on differences and homologies with respect to other types of MR. The ultimate goal is to find out a common roadmap in view of future therapeutical approaches to MR. Particular attention will be devoted to: a) structural and functional anomalies of dendrites b) derangement and rewiring of cortical and hippocampal microcircuits c) involvement of non-cortical brain structures d) apoptosis and/or altered neurogenesis e) anomalies of ion channels, neurotransmitters, and neurotrophic factors f) comparison between experimental studies and imaging studies performed on humans affected by FASD.
    Sprache: Englisch
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    HU Berlin
    FU Berlin
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  • 7
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    Online-Ressource
    Obesity-induced inflammation and insulin resistance / (2015)
    France :Frontiers Media SA,
    Details
    UID:
    almafu_9958122662602883
    Umfang: 1 online resource (120 pages) : , digital, PDF file(s).
    ISBN: 9782889193080
    Serie: Frontiers Research Topics
    Inhalt: Obesity-induced chronic inflammation is crucial in the pathogenesis of insulin resistance, type 2 diabetes, and the metabolic syndrome. Obesity-associated systemic inflammation is characterized by increased circulating concentrations of proinflammatory cytokines and chemokines, and activation of pathways that regulate inflammation, including JNK and IKKβ/NF-κB pathways. A significant advance in our understanding of obesity-associated inflammation and insulin resistance has been recognition of the critical role of adipose tissue macrophages (ATMs) in both mice and humans. ATMs are a prominent source of proinflammatory cytokines, such as TNF-α and IL-6, that can block insulin action in adipose tissue, skeletal muscle, and liver autocrine/paracrine signalling and cause systemic insulin resistance via endocrine signalling, providing a potential link between inflammation and insulin resistance. Although the initiating factors of this inflammatory response remains to be fully determined, accumulating evidence supports that obesity-induced inflammation is mainly mediated by immune cells. Immune response and metabolic regulation are highly integrated and this interface maintains a central homeostatic system, dysfunction of which can cause obesity-associated metabolic diseases such as type 2 diabetes and cardiovascular disease. However, the links between nutrient sensing systems and the interface of metabolic and inflammatory responses are complex. Particularly, it is not clear how obesity or nutrient excess first regulates subsets of immune cells in circulation and induces local inflammation, including the recruitment and activation of ATMs. Furthermore, it is not determined in which cells or tissues inflammation initially occurs upon obesity, which then causes systemic inflammation and subsequent development of insulin resistance. The Research Topic is to highlight the interconnection between obesity, inflammation, and insulin resistance. We encourage interested scientists to submit mini-reviews, methods papers, review articles, perspectives, and original research articles covering this topic in all its diversity to appreciate the mechanisms of obesity-induced inflammation and role of immune system in the pathogenesis of obesity and diabetes.
    Anmerkung: Bibliographic Level Mode of Issuance: Monograph , English
    Sprache: Englisch
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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    HU Berlin
    FU Berlin
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  • 8
    Online-Ressource
    Online-Ressource
    New treatment perspectives in autism spectrum disorders / (2015)
    France :Frontiers Media SA,
    Details
    UID:
    almafu_9958106754502883
    Umfang: 1 online resource (161 pages) : , illustrations; digital file(s).
    ISBN: 9782889193080
    Serie: Frontiers Research Topics
    Inhalt: Developing novel and more effective treatments that improve quality of life for individuals with autism spectrum disorders is urgently needed. To date a wide range of behavioral interventions have been shown to be safe and effective for improving language and cognition and adaptive behavior in children and adolescents with ASD. However many people with ASD can receive additional benefit from targeted pharmacological interventions. One of the major drawback in setting up therapeutics intervention is the remarkable individual differences found across individuals with ASD. As a matter of fact the medications that are currently available address only symptoms associated with ASD and not the core domains of social and communication dysfunction. The pathogenesis paradigm shift of ASD towards synaptic abnormalities moved the research to pathway to disease that involve multiple systems and that are becoming the forefront of ASD treatment and are pointing toward the development of new targeted treatments. Some new therapeutics have been tested and others are being studied. In this context single gene disorders frequently associated with ASD such as Rett Syndrome, Fragile X and Tuberous Sclerosis have been of significant aid as neurobiology of these disorders is more clear and has a potential to shed light on the altered signalling in ASD. However much research is needed to further understand the basic mechanisms of disease and the relationship to idiopathic ASD. Clinical trials in children are underway with agents directed to core symptoms and to the associated disorders in the search of new therapeutics and progress are expected with possible new option for therapeutics in ASD in the upcoming future. Children and Adolescents with ASD and their families can provide important information about their experience with new treatments and this should be a priority for future research. In addition, research performed on genetic mouse models of ASD will keep on providing useful information on the molecular pathways disrupted in the disease, thus contributing to identify novel drug targets.
    Anmerkung: Bibliographic Level Mode of Issuance: Monograph , English
    Sprache: Englisch
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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    HU Berlin
    FU Berlin
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  • 9
    Online-Ressource
    Online-Ressource
    Harnessing oncolytic virus-mediated immunity / (2015)
    Switzerland :Frontiers Media SA,
    Details
    UID:
    almafu_9958116396602883
    Umfang: 1 online resource (110 pages) : , illustrations; digital, PDF file(s).
    ISBN: 9782889193080 (ebook)
    Serie: Frontiers Research Topics
    Inhalt: Oncolytic viruses (OVs) have emerged as a promising anticancer treatment. OVs selectively infect, replicate in, and kill tumor cells. Oncolytic viral therapy occurs in two phases: an initial phase where the virus mediates direct oncolysis of tumor cells, and a second phase where an induced post-oncolytic immune response continues to mediate tumor destruction and retards progression of the disease. For a long time, the therapeutic efficacy was thought to depend mainly on the direct viral oncolysis based on their tumor selective replication and killing activities. But the post-oncolytic anti-tumor activity induced by the OV therapy is also a key factor for an efficient therapeutic activity. The topic addresses various strategies how to optimize OVs anti-tumor activity.
    Anmerkung: Bibliographic Level Mode of Issuance: Monograph , English
    Sprache: Englisch
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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    Online-Ressource
    HU Berlin
    FU Berlin
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  • 10
    Online-Ressource
    Online-Ressource
    Levodopa-induced dyskinesias in Parkinson's disease : current knowledge and future scenarios (2015)
    France :Frontiers Media SA,
    Details
    UID:
    almafu_9958122666002883
    Umfang: 1 online resource (99 pages) : , illustrations; digital file(s).
    ISBN: 9782889193080
    Serie: Frontiers Research Topics
    Inhalt: Levodopa-induced dyskinesias (LID) are abnormal movements that occur during the period of maximal benefit of parkinsonian symptoms when levodopa concentration in the brain is highest. LID are mainly choreic in nature and represent a very common problem in up to 80% of Parkinson’s disease (PD) patients treated with levodopa. Current knowledge highlights the critical involvement of the striato-thalamo-cortical pathways, which are characterized by abnormal physiological overactivity. However, despite many recent advances in genetic and pharmacological fields, the pathophysiological mechanisms underlying LID are still a matter of debateIn the last few years, advances in the neurophysiological and neuroimaging fields have provided alternative scenarios for understanding the neurobiological mechanisms of LID. Indeed, several lines of evidence support the notion that others structures, outside traditional striato-thalamo-cortical pathways, are strongly involved in the LID. In particular, the cerebello-thalamic circuitry as well as intra-cortical connections between the premotor cortex (particularly supplementary motor area) and the inferior frontal cortex, would seem to play a key role in the dysfunctional pathophysiological model of LID.This topic aims to pool the most recent advances in the phenomenology and pathophysiology of levodopa-induced dyskinesias. We aim to compile original research papers, review articles, technical reports and commentaries that cover this topic broadly. Researchers with interest in clinical aspects (and particularly management strategies, e.g. deep-brain stimulation), neuroimaging (using either functional or structural MRI approaches), neurophysiology (transcranial magnetic stimulation (TMS)) of LID and other hyperkinetic movement disorders (i.e., dystonia, Huntington's disease, Gilles de la Tourette's syndrome), are encouraged to contribute to this topic. Again, articles concerning animal models of PD will be particularly appreciated.
    Anmerkung: Bibliographic Level Mode of Issuance: Monograph , English
    Sprache: Englisch
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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    HU Berlin
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