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The role of viable but non-infectious developmental forms in chlamydial biology

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193219 Year: Pages: 119 DOI: 10.3389/978-2-88919-321-9 Language: English
Publisher: Frontiers Media SA
Subject: Internal medicine --- Science (General)
Added to DOAB on : 2016-02-05 17:24:33
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The chlamydiae are Gram-negative, obligate intracellular bacteria with a complex developmental cycle comprising a metabolically less-active, infectious stage, the elementary body (EB), and a metabolically more active stage, the reticulate body (RB). They are responsible for many acute and chronic diseases in humans and animals. In order to play a causative role in chronic diseases, chlamydiae would need to persist and to re-activate within infected cells/tissues for extended periods of time. Persistence in vitro is defined as viable but non-cultivable chlamydiae involving morphologically enlarged, aberrant, and nondividing RBs, termed aberrant bodies (AB). In vitro, alterations of the normal developmental cycle of chlamydiae can be induced by the addition of Interferon-? (IFN-?), tumor necrosis factor-a (TNF-a) and penicillin G exposure as well as amino acid or iron deprivation, monocyte infection and co-infection with viruses. In vivo, key questions include whether or not ABs occur in infected patients and animals and whether such ABs can contribute to prolonged, chronic inflammation, fibrosis, and scarring through continuing stimulation of the host immune system known from diseases such as trachoma, pelvic inflammatory disease, reactive arthritis and atherosclerosis. To date, the direct causal role in the pathogenesis of chlamydial infection and persistence in vivo has been questioned since there was no tractable animal model of chlamydial persistence so far. A very recent study was able to establish an experimental animal model of in vivo persistence, when C. muridarum vaginally-infected mice were gavaged with amoxicillin. Amoxicillin treatment induced C. muridarum to enter the persistent state in vivo. Recent in vivo data from patients indicate that viable but non-infectious developmental stages are present in the genital tract of chronically-infected women and that the gastrointestinal tract might be a reservoir for persistent chlamydial infections at other sites.

Natural Killer Cells in Human Diseases: Friends or Foes?

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889454044 Year: Pages: 122 DOI: 10.3389/978-2-88945-404-4 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2018-11-16 17:17:57
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NK cells are lymphocytes of the innate immune system that share some features with adaptive immune cells like T cells. They are well known for their importance to control viral infections and tumor development, but also intracellular bacterial and parasitic infections. A balance between negative and positive signals transmitted via germ line-encoded inhibitory and activating receptors controls the function of NK cells. Activated NK cells respond by killing the infected or tumor cells without prior sensitization, and by producing cytokines and chemokines. It has been shown that NK cells cross-talk with other immune cells, such as dendritic cells and macrophages, can shape T cell and B cell immune responses through direct interactions as well as by virtue of their cytokine/chemokine production. NK cells can also regulate immune responses by killing other immune cells, including activated T cells, or by producing anti-inflammatory cytokines upon excessive inflammation. However, NK cells are not friends in all situations. Indeed, it has been shown in LCMV-infected murine models that, depending on the viral inoculation load, NK cells may either help fight infection or can promote chronic infection. Moreover in cancer models, it has been shown that NK cells can kill anti-tumoral T cells. Recent studies of NK cells in patients with cancer support the notion of detrimental roles of NK cells. Furthermore, studies implicate NK cells in contributing to both graft rejection and tolerance to an allograft. In some autoimmune diseases, like rheumatoid arthritis, NK cells may promote disease pathogenesis. The scope of this Research Topic is to present and discuss knowledge on the role of NK cells in various diseases settings: viral infections as well as other infections, cancer, transplantation, and autoimmunity. The aim is to discuss how NK cells respond during disease and specifically when, why and how NK cells can be harmful and if they exert different functions (production of specific cytokines, inhibition of other immune cells through other mechanisms beside cytotoxicity) in these situations. Which are the NK cell subsets that play beneficial or deleterious roles in these diseases? Are there different phenotypes associated with protective NK cells (e.g. antiviral, antitumoral) and NK cells involved in disease pathogenesis? How are these diverse NK cells activated and do they function primarily through direct cytotoxicity, ADCC or cytokine and chemokine production? What are the signals or interactions that can change and shape the NK cell response shifting them from protective to harmful? We thank the authors that submitted reviews and original research manuscripts that help to better understand these questions, with the aim that this will help the scientific community to determine what could be the main future research directions to better understand the role of NK cells in disease protection or development.

Chromatin & Transcriptional Tango on the Immune Dance Floor

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889195107 Year: Pages: 144 DOI: 10.3389/978-2-88919-510-7 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2015-12-03 13:02:24
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Signaling through the cell surface antigen receptor is a hallmark of various stages of lymphocyte development and adaptive immunity. Besides the adaptive immune system, the innate immunity is equally important for protection. However, the mechanistic connection between signaling, chromatin changes and downstream transcriptional pathways in both innate and adaptive immune system remains incompletely understood in hematopoiesis. A related issue is how the enhancers communicate to the promoters in a stage specific fashion and in the context of chromatin. Because the factors that regulate chromatin are generally present and active in most cell types, how could cell type and/or stage specific chromatin architecture is achieved in response to a particular immune signal?The genetic loci that encode lymphocyte cell surface receptors are in an "unrearranged” or “germline” configuration during the early stages of development. Thus, in addition to expressing lineage and/or stage specific transcription factors during each developmental stage, lymphocytes also need to rearrange their cognate receptor loci in a strictly ordered fashion. Hence, there must be a tightly coordinated communication between the recombination machinery and the transcriptional machinery (including chromatin regulators) at every developmental step. Mature B cells also undergo classswitch recombination and somatic hypermutation. Importantly, along the way, these cells must avoid autoimmune responses and only those cells capable of recognizing foreignantigens are preserved to reach peripheral organs where they must function. The exquisite regulation that govern chromatin accessibility, recombination and transcription regulation in response to the environmental signals in the immune system is discussed here is a series of articles.

Post-Exercise Recovery: Fundamental and Interventional Physiology

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889198559 Year: Pages: 78 DOI: 10.3389/978-2-88919-855-9 Language: English
Publisher: Frontiers Media SA
Subject: Physiology --- Science (General)
Added to DOAB on : 2016-01-19 14:05:46
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Physiological responses after maximal and submaximal exercise are routinely monitored in a plethora of diseases (e.g. cardiovascular diseases, cancer, diabetes, asthma, neuromuscular disorders), and normal populations (e.g. athletes, youth, elderly), while slower or irregular post-exercise recovery usually indicates poor health and/or low fitness level. Abnormal post-exercise recovery (as assessed via blunted post-exercise heart rate dynamics) helps to predict the presence and severity of coronary artery disease, while differences in recovery outcomes in athletes might discriminate between fit and unfit individuals. Disturbances in post-exercise recovery might be due to acute or persistent changes in: (1) adaptive responses mediated by the autonomic nervous system and vasodilator substances, (2) cellular bioenergetics, and/or (3) muscular plasticity. Preliminary evidence suggests possible role of time-dependent modulation of nitric oxide synthase and adenosine receptors during post-exercise recovery, yet no molecular attributes of post-exercise recovery are revealed so far. Currently several markers of post-exercise recovery are used (e.g. heart rate measures, hormone profiles, biochemical and hematological indices); however none of them meets all criteria to make its use generally accepted as the gold standard. In addition, recent studies suggest that different pharmacological agents and dietary interventions, or manipulative actions (e.g. massage, cold-water immersion, compression garments, athletic training) administered before, during or immediately after exercise could positively affect post-exercise recovery. There is a growing interest to provide more evidence-based data concerning the effectiveness and safety of traditional and novel interventions to affect post-exercise recovery. The goals of this research topic are to critically evaluate the current advances on mechanisms and clinical implications of post-exercise recovery, and to summarize recent experimental data from interventional studies. This knowledge may help to identify the hierarchy of key mechanisms, and recognize methods to monitor and improve post-exercise recovery in both health and disease.

Pathogenesis of Leptospira

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889456499 Year: Pages: 103 DOI: 10.3389/978-2-88945-649-9 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Internal medicine
Added to DOAB on : 2019-01-23 14:53:43
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The present eBook, consisting of a compilation of research and review articles, focuses on the features and mechanisms adopted and explored by pathogenic leptospires to successfully establish infection in the host. Additionally, this eBook provides information to support future work focused on the development of new prevention approaches against this important yet neglected zoonotic disease.

Industrial and Host Associated Stress Responses in Food Microbes. Implications for Food Technology and Food Safety

Authors: --- --- --- --- et al.
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889452934 Year: Pages: 295 DOI: 10.3389/978-2-88945-293-4 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Microbiology
Added to DOAB on : 2018-02-27 16:16:44
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Throughout the food processing chain and after ingestion by the host, food associated bacteria have to cope with a range of stress factors such as thermal and/or non-thermal inactivation treatments, refrigeration temperatures, freeze-drying, high osmolarity, acid pH in the stomach or presence of bile salts in the intestine, that threaten bacterial survival. The accompanying plethora of microbial response and adaptation phenomena elicited by these stresses has important implications for food technology and safety. Indeed, while resistance development of pathogenic and spoilage microorganisms may impose health risks for the consumer and impart great economic losses to food industries, reduced survival of probiotic bacteria may strongly compromise their claimed health benefit attributes. As a result, substantial research efforts have been devoted in the last decades to unravel the mechanisms underlying stress response and resistance development in food associated microorganisms in order to better predict and improve (i) the inactivation of foodborne pathogens and spoilage microorganisms on the one hand and (ii) the robustness and performance of beneficial microorganisms on the other. Moreover, the recent implementation of system-wide omics and (single-)cell biology approaches is greatly boosting our insights into the modes of action underlying microbial inactivation and survival. This Research Topic aims to provide an avenue for dissemination of recent advances within the field of microbial stress response and adaptation, with a particular focus not only on food spoilage and pathogenic microorganisms but also on beneficial microbes in foods.

Lademanagement für Elektrofahrzeuge

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ISBN: 9783731505655 Year: Pages: XIII, 209 DOI: 10.5445/KSP/1000057827 Language: GERMAN
Publisher: KIT Scientific Publishing
Subject: Business and Management
Added to DOAB on : 2019-07-30 20:02:02
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The present work describes a charging management with integrated charging optimization for electric vehicles that can be provided to a fleet by a fleet operator or to a group of private customers by a loading infrastructure operator. Aim of this charging optimization is the calculation of an optimized charging plan by considering the electricity price as well as hard capacity boundaries and user requirements. This charging optimization is designed and implemented within the scope of this work.

Control of Visceral Leishmaniasis by Immunotherapeutic and Prophylactic Strategies

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889195527 Year: Pages: 144 DOI: 10.3389/978-2-88919-552-7 Language: English
Publisher: Frontiers Media SA
Subject: Public Health --- Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2016-01-19 14:05:46
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Visceral leishmaniasis (VL) or kala-azar is the most dreadful of all forms of leishmaniasis caused by Leishmania donovani in Old World and Leishmania chagasi and/or Leishmania infantum in New World affecting millions of people worldwide. In active VL, macrophages host the replicating amastigotes in phagolysosomal compartments leading to splenomegaly, hepatomegaly, hyperglobulinemia, anemia, weight-loss, incessant fever and ultimately death if not treated. Treatments available against the disease are limited by increased incidence of resistance, serious side-effects, high cost and long course of treatment. Immuno-chemotherapy is an alternative to overcome the limitations of the drugs against VL. Combination of one or more of immunotherapeutic agents like BCG, Alum, IFN-?, antigen-pulsed dendritic cells (DC), etc. with chemotherapeutic drugs have been tested raising hopes for a suitable immuno-chemotherapy against VL and Post Kala-azar Dermal Leishmaniasis (PKDL). Antagonists of IL-10, TGF-ß, IL-13 have been effectively used with pentavalent antimonials in treatment of experimental VL. Some parasitic antigens and liposomal formulations have also been shown to impart superior therapeutic effectiveness to antileishmanial drugs. For socio-economic reasons prophylaxis is always more desirable than therapy. Although no vaccine against any form of leishmaniasis in humans is available, patients successfully treated show considerable protection from reinfection highlighting the possibility of developing prophylactic measures against the disease. Subsequently a lot of interest has been focused recently towards developing vaccines against VL and many potential vaccine candidates like whole cell (attenuated or heat killed), crude fractions, purified subunits, DNAs, recombinant proteins, fusion proteins, and genetically modified live attenuated parasites etc. have been reported. These vaccine candidates are either activators of CD4+Th1 cells and/or CD8+ T cells or neutralizers of immuno-suppression. Cationic liposomal formulations, nanoparticle and virosome delivery systems, etc. have been used to increase potency and durability of various vaccine candidates. Immuno-modulators like TLR agonists have been shown to be promising adjuvants in enhancing efficacy and overcoming the challenge of human administrable vaccine formulations. Recently role of sand fly salivary gland proteins as immune-modulators also has been explored. Various strategies such as heterologous prime boosting, targeted antigen delivery, adjuvant mediated protection, have been undertaken. Likewise, precise role of regulatory T cells (Tregs) in VL disease progression needs to be investigated and exploited to develop both immuno-therapeutic and prophylactic methods. A breakthrough in immunotherapy and prophylactic strategy would help in eradication of the parasites from the pool of natural reservoirs namely VL and PKDL patients, asymptomatic carrier individuals and infected dogs ensuring success of global VL control programs.

Endoplasmic Reticulum Stress Response and Transcriptional Reprogramming

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889194360 Year: Pages: 97 DOI: 10.3389/978-2-88919-436-0 Language: English
Publisher: Frontiers Media SA
Subject: Genetics --- Science (General)
Added to DOAB on : 2016-01-19 14:05:46
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Endoplasmic reticulum (ER) is an intracellular organelle responsible for protein folding and assembly, lipid and sterol biosynthesis, and calcium storage. A number of biochemical, physiological, or pathological stimuli can interrupt protein folding process, causing accumulation of unfolded or misfolded proteins in the ER lumen, a condition called “ER stress”. To cope with accumulation of unfolded or misfolded proteins, the ER has evolved a group of signaling pathways termed “Unfolded Protein Response (UPR)” or “ER stress response” to align cellular physiology. To maintain ER homeostasis, transcriptional regulation mediated through multiple UPR branches is orchestrated to increase ER folding capacity, reduce ER workload, and promote degradation of misfolded proteins. In recent years, accumulating evidence suggests that ER stress-triggered transcriptional reprogramming exists in many pathophysiological processes and plays fundamental roles in the initiation and progression of a variety of diseases, such as metabolic disease, cardiovascular disease, neurodegenerative disease, and cancer. Understanding effects and mechanisms of ER stressassociated transcriptional reprogramming has high impact on many areas of molecular genetics and will be particularly informative to the development of pharmacologic avenues towards the prevention and treatment of modern common human diseases by targeting the UPR signaling. For these reasons, ER stress response and transcriptional reprogramming are a timely and necessary topic of discussion for Frontiers in Genetics.The important topics in this area include but not limited to:(1) ER-resident transcription factors and their involvements in ER stress response and cell physiology; (2) Physiologic roles and molecular mechanisms of ER stress-associated transcriptional regulation in lipid and glucose metabolism; (3) In vitro and in vivo models for ER stress-associated transcriptional reprogramming; (4) ER stress-associated transcriptional regulation in human disease; (5) Therapeutic potentials by targeting ER stress response pathways.

Neuronal Self-Defense: Compensatory Mechanisms in Neurodegenerative Disorders

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197590 Year: Pages: 190 DOI: 10.3389/978-2-88919-759-0 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-04-07 11:22:02
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Neurodegenerative disorders are characterized by the progressive loss of specific populations of neurons with consequent deterioration of brain's function and dramatic impact on human behavior. At present, there are no effective cures for neurodegenerative diseases. Because unambiguous diagnosis is possible only after manifestation of symptoms, when a large proportion of neurons has been already lost, therapies are necessarily confined to alleviation of symptoms. Development of cures halting the disease course is hampered by our rudimentary understanding of the etiopathology. Most neurodegenerative disorders are sporadic and age-related and - even for those of known genetic origin - the mechanisms influencing disease onset and progression have not been fully characterized. The different diseases, however, share important similarities in the mechanisms responsible for neuronal loss, which is caused by a combination of endogenous and exogenous challenges. Trophic deprivation, oxidative stress, accumulation of abnormal protein aggregates, and bioenergetics defects have been described in most, if not all, neurodegenerative disease. To counterbalance these noxious stimuli cells deploy, at least during the initial pathogenic states, intrinsic neuroprotective responses. These are general compensatory mechanisms, common to several neurodegenerative conditions, which reprogram cellular physiology to overcome stress. Adaptation includes strategies to optimize energetic resources, for instance reduction of rRNA synthesis to repress translation, suppression of transcription, and bioenergetics and metabolic redesign. Additional mechanisms include potentiation of antioxidant capacity, induction of endoplasmic reticulum (ER) stress, and activation of protein quality control systems and autophagy. Ineffective execution of these compensatory strategies severely threatens cellular homeostasis and favors onset of pathology. Therefore, a better understanding of these "buffering" mechanisms and of their interconnections may help to devise more effective therapeutic tools to prolong neuronal survival and activity, independently of the original genetic mutations and stress insults. This Research Topic focuses on the initial compensatory responses protecting against failure of those mechanisms that sustain neuronal survival and activity. The collection intends to summarize the state-of-the-art in this field and to propose novel research contributes, with the ultimate goal of inspiring innovative studies aimed to contrast progression of neurodegenerative diseases.

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