Inflammatory Bowel Disease PDF Download
Are you looking for read ebook online? Search for your book and save it on your Kindle device, PC, phones or tablets. Download Inflammatory Bowel Disease PDF full book. Access full book title Inflammatory Bowel Disease by Stephan R. Targan. Download full books in PDF and EPUB format.
Author: Stephan R. Targan
Publisher: John Wiley & Sons
ISBN: 1444359118
Category : Medical
Languages : en
Pages : 1429
Get Book Here
Book Description
This is the state-of–the-art book on inflammatory bowel disease you have been waiting for Written and edited by international experts in gastroenterology this up-to-date volume provides a complete review of the basic science behind inflammatory bowel disease (IBD), as well as evidence-based clinical guidance on diagnosis, treatment and long-term management of IBD. In 50 chapters the authors cover the latest and most promising treatment modalities and the science behind them. There are chapters which cover the advances in the medical and surgical treatment of conditions such as Crohn's disease and ulcerative colitis, as well as chapters focusing on nutrition, imaging and complementary medicine. This is an invaluable information resource for all those in the medical team treating patients with IBD. Whether you are a gastroenterologist, gastrointestinal surgeon or GI nurse specialist this book deserves a place in your library.
Author: Stephan R. Targan
Publisher: John Wiley & Sons
ISBN: 1444359118
Category : Medical
Languages : en
Pages : 1429
Get Book Here
Book Description
This is the state-of–the-art book on inflammatory bowel disease you have been waiting for Written and edited by international experts in gastroenterology this up-to-date volume provides a complete review of the basic science behind inflammatory bowel disease (IBD), as well as evidence-based clinical guidance on diagnosis, treatment and long-term management of IBD. In 50 chapters the authors cover the latest and most promising treatment modalities and the science behind them. There are chapters which cover the advances in the medical and surgical treatment of conditions such as Crohn's disease and ulcerative colitis, as well as chapters focusing on nutrition, imaging and complementary medicine. This is an invaluable information resource for all those in the medical team treating patients with IBD. Whether you are a gastroenterologist, gastrointestinal surgeon or GI nurse specialist this book deserves a place in your library.
Author: Charles N. Serhan
Publisher: Cambridge University Press
ISBN: 1139936670
Category : Science
Languages : en
Pages : 489
Get Book Here
Book Description
The acute inflammatory response is the body's first system of alarm signals that are directed toward containment and elimination of microbial invaders. Uncontrolled inflammation has emerged as a pathophysiologic basis for many widely occurring diseases in the general population that were not initially known to be linked to the inflammatory response, including cardiovascular disease, asthma, arthritis, and cancer. To better manage treatment, diagnosis, and prevention of these wide-ranging diseases, multidisciplinary research efforts are underway in both academic and industry settings. This book provides an introduction to the cell types, chemical mediators, and general mechanisms of the host's first response to invasion. World-class experts from institutions around the world have written chapters for this introductory text. The text is presented as an introductory springboard for graduate students, medical scientists, and researchers from other disciplines wishing to gain an appreciation and working knowledge of current cellular and molecular mechanisms fundamental to inflammation.
Author: Kevin Christopher Barry
Publisher:
ISBN:
Category :
Languages : en
Pages : 118
Get Book Here
Book Description
Translating inflammation: characterization of host protein synthesis during bacterial infections by Kevin Christopher Barry Doctor of Philosophy in Molecular and Cell Biology University of California, Berkeley Professor Russell E. Vance, Chair The innate immune system is the first line of defense against pathogens. Innate immune receptors, termed pattern recognition receptors, are germline-encoded receptors that recognize conserved microbial products and activate an immune response. Examples of these microbial products, termed pathogen-associated molecular patterns, are components of the bacterial outer membrane, such as lipopolysaccharide or bacterial lipoproteins, and microbe-derived nucleic acids. Importantly these molecular patterns are not just found on pathogens, but are also encoded by harmless commensal microbes as well. It has become clear in recent years that the innate immune system distinguishes pathogens from harmless commensals and preferentially responds to pathogens. It has been established that one mechanism by which the innate immune system makes this distinction is through the recognition of activities that are associated with the pathogenic lifestyle, termed patterns of pathogenesis, such as access to the host cytosol and microbial growth. Recently, translation inhibition induced by pathogenic microbes has been shown to be important for the induction of immune responses, and thus has been termed a novel pathogen-associated activity. Legionella pneumophila is a gram-negative intracellular bacterial pathogen that is the causative agent of a severe pneumonia called Legionnaires' Disease. After inhalation of aerosolized bacteria, L. pneumophila can infect and replicate within lung alveolar macrophages. Intracellular replication of L. pneumophila in macrophages in vitro, and virulence of L. pneumophila in animal models, requires a Type IV secretion system (T4SS) called the Dot/Icm system, which secretes bacterial effector proteins into the host cytosol. These effectors, greater than 270 of which have been identified, are believed to be critical for establishment of the Legionella-containing vacuole, the specialized membrane-bound intracellular compartment in which L. pneumophila replicates. In addition to its essential role in facilitating intracellular bacterial replication, the L. pneumophila T4SS is also associated with a strong block in host protein synthesis and the induction of several potent innate immune responses. The over-arching goal of this thesis is to expand our knowledge of the mechanisms by which the innate immune system distinguishes pathogenic microbes from non-pathogenic microbes. In the first chapter of this thesis I will review the current state of the field. In the second chapter of this thesis I will describe studies using L. pneumophila infection in vivo where I found an important role for the often-overlooked cytokine, interleukin-1[alpha] (IL-1[alpha]), in initiating the immune response to virulent L. pneumophila. I was able to demonstrate, consistent with previous studies, that signaling through the interleukin-1 receptor (IL-1R) is important for the recruitment of protective neutrophils to the lungs of mice, but unlike previous studies, we could show that the early recruitment of these cells required IL-1[alpha]. I was further able to characterize the molecular mechanism by which the innate immune system is able to produce IL-1[alpha] specifically in response to virulent infection. I found that host protein synthesis is inhibited by T4SS+, but not T4SS-, L. pneumophila. I was further able to show that translation inhibition in concert with signaling via the innate immune receptors the toll-like receptors (TLRs) induced sustained and massive induction of Il1a transcript. I proposed that this massive induction of Il1a transcript overcame the L. pneumophila induced block in host protein synthesis and permitted the enhanced production and release of IL-1[alpha]. Thus, these studies demonstrated that IL-1[alpha], a cytokine I showed to be important for protecting the host from L pneumophila infection in vivo, was preferentially made in response to T4SS+ L. pneumophila. Moreover, I linked the production of IL-1[alpha] to the sensing of the pathogen-induced block in host protein synthesis. These studies also identified five known and two novel bacterial effectors that block host protein synthesis, but deletion of all seven of these effectors did not affect the L. pneumophila induced block in host protein synthesis. I hypothesized that other mechanisms, possibly host stress induced by intracellular bacterial infection, could induce this block in translation. Thus, taken together, the experiments described in the second chapter of this thesis identify a novel inflammatory response to L. pneumophila in vivo and further support a model in which pathogen-induced translation inhibition can allow the immune system to detect a pathogen and respond appropriately. In the third chapter of this thesis I set out to further characterize the molecular mechanism of IL-1[alpha] production and translation inhibition induced by T4SS+ L. pneumophila. As deletion of the seven L. pneumophila effectors that block host protein synthesis did not relieve the block in host protein synthesis induced by L. pneumophila, I set out to determine if the residual block in host protein synthesis by the [Delta]7 L. pneumophila mutant was at the level of translation initiation or elongation. Using a deep sequencing technique called ribosome profiling in concert with RNAseq of total mRNA, I was able to look at translation in L. pneumophila infected macrophages globally and with nucleotide resolution. I found through these analyses that T4SS+ L. pneumophila blocks translation elongation, but the residual translation inhibition induced by [Delta]7 L. pneumophila was at the level of translation initiation. The vast majority of translational control by the host is at the level of translation initiation. Thus, the [Delta]7 L. pneumophila induced block in translation initiation suggests that a host stress response could be blocking translation in response to the stresses of being infected by an intracellular pathogen. In the third chapter of this thesis I assay a number of host stress response pathways after L. pneumophila infection and see no role for these pathways in [Delta]7 L. pneumophila induced translation inhibition. I proposed that these data suggest that an unknown stress response pathway may be activated or, alternatively, a novel bacterial effector could be blocking translation initiation. The studies described in the third chapter of this thesis also undertook analyses of ribosome profiling and RNAseq data to further test the model that inflammatory cytokines are made in response to pathogens by the massive induction of transcripts in response to the pathogen-associated activity of blocking host protein synthesis along with TLR signaling. The data presented in the third chapter support a model that the induction of cytokine transcripts via sensing of the pathogen-associated activity of translation inhibition and TLR activation overcomes the block in host protein synthesis and allows the infected cell to preferentially respond to pathogens with the production of inflammatory cytokines. I further describe experiments that suggest diverse intracellular bacterial pathogens such as Listeria monocytogenes also induce a block in host protein synthesis and that this activity may be a broadly applicable pathogen-associated activity. Lastly, the studies presented in the third chapter of this thesis provide evidence that, at least in response to virulent L. pneumophila, the majority of control of gene expression in response to pathogenic infection is controlled at the level of mRNA induction. The studies presented in this thesis lend credence to the proposal that translation inhibition is a pathogen-associated activity encoded by diverse intracellular bacterial pathogens. They also support a model by which translation inhibition is sensed by host innate immune cells to induce massive mRNA induction of inflammatory cytokines allowing for a specific inflammatory response to pathogens. Lastly, these studies link translation inhibition to an important role in protecting the host from pathogenic infection in vivo.
Author: B. Vucelic
Publisher: Springer Science & Business Media
ISBN: 9781402028472
Category : Medical
Languages : en
Pages : 314
Get Book Here
Book Description
The amount of information on the pathogenesis of inflammatory bowel disease is growing rapidly. This is reflected by a continuous increase in the number of papers presented at international GI meetings. To make things more difficult for practicing physicians, there is also a large number of new clinical trials being published which require periodical critical reviews and recommendations. Faced with these issues, the scientific commitee of the Falk Symposium No. 140 decided to take a different approach and to apply a novel format that is reflected in the title of the Symposium: "Translation from basic research to clinical practice". This book contains the proceedings of that Symposium, held in Dubrovnik, Croatia, on May 7–8, 2004. The sections are designed so that they start with the information from basic sciences on different aspects of these complex diseases and further lead to their clinical implications. Special attention is paid to the mechanisms of actions of established drugs. The last two sections are clinically oriented and focus on the most difficult aspects of both Crohn's disease and ulcerative colitis. This format provides state-of-the-art chapters by leading experts in the field and at the same time up-to-date information on the clinical application of the new knowledge.
Author: Fleurtje Marieke Valk
Publisher:
ISBN: 9789462994188
Category :
Languages : en
Pages : 0
Get Book Here
Book Description
Author: Dakang Xu
Publisher: Springer
ISBN: 981105987X
Category : Medical
Languages : en
Pages : 254
Get Book Here
Book Description
This book discusses recent research in innate immunity, which has revealed a large number of receptors that sense the presence of microorganisms or cellular damage in tissues. In complex tissues, many of these sensing events occur simultaneously. Thus, the downstream signaling pathways need to be integrated so that an appropriate cellular inflammatory response can be initiated. In addition, the inflammasome defines the molecular and cellular processes of inflammation in response to microbial infection. Previous data suggested that regulation of inflammasomes is mediated by microbes, but inflammasomes also have antimicrobial functions. Increasing evidence in mouse models, together with human data, strongly implicates an involvement of the inflammasome and uncontrolled inflammation in the initiation and progression of diseases with a high impact on public health. The book reviews novel aspects of functional genomics, epigenomics, transcriptomics, post-translat ional modifications, microbiome and immunometabolism in order to understand inflammatory signaling and responses, covering recent findings on the mechanisms underlying the regulation of inflammatory responses to pathogens, dysregulation of these responses in inflammatory disease, and the use of such mechanisms to boost or subdue the inflammatory response. Bridging the gaps in understanding between the fields of human and mouse immunology, it provides valuable insights into inflammatory-mediated disease and immune defense. Such innovative perspectives in both basic and clinical research promote the translation of knowledge to the clinic.
Author: Yoram Vodovotz
Publisher: Springer Science & Business Media
ISBN: 1461480086
Category : Science
Languages : en
Pages : 288
Get Book Here
Book Description
The difficulty in achieving effective translation of basic mechanistic biomedical knowledge into effective therapeutics, is the greatest challenge in biomedical research. Nowhere is this more apparent than in the reductionist approaches to understanding and manipulating the acute inflammatory response in the settings of sepsis, trauma/hemorrhage, wound healing, and related processes. This book discusses complex systems and computational biology methods and approaches that have advanced sufficiently to allow for knowledge generation, knowledge integration, and clinical translation in the settings of complex diseases related to the inflammatory response. Well-regulated, self-resolving inflammation is necessary for the appropriate communication and resolution of infection and trauma, and for maintenance of proper physiology and homeostasis. In contrast, self-sustaining inflammation drives the pathobiology of the aforementioned diseases. It is now increasingly recognized that controlling and reprogramming inflammation in order to reap the benefits of this evolutionarily-conserved process is preferred to simply abolishing indiscriminately.
Author: Elie Metchnikoff
Publisher:
ISBN:
Category : Inflammation
Languages : en
Pages : 302
Get Book Here
Book Description
Metchnikoff's classical lectures on the pathology of inflammation appeared in Russian in 1892. The book was translated into French the same year, and the next year the English translation appeared. -- H.W. Orr.
Author: Bruce Alberts
Publisher:
ISBN: 9780815332183
Category : Cytology
Languages : en
Pages : 0
Get Book Here
Book Description
Author: Peter B. Soeters
Publisher: Academic Press
ISBN: 0128204222
Category : Science
Languages : en
Pages : 336
Get Book Here
Book Description
Reciprocal Translation Between Pathophysiology and Practice in Health and Disease brings a novel perspective, closing the knowledge gap between normal/abnormal physiology. Chapters describe the basic mechanisms underlying a disease or trauma-related response, describe consequences in practice, and provide insights on how to use information to better understand disease outcomes. Other sections explore how these responses are beneficial and driven by similar hormones and inflammatory immune cell derived modulators. This is a must-have resource for those seeking an authoritative and comprehensive understanding on how to treat the basic mechanisms underlying disease or trauma-related responses.With contributions from Petronella L.M. Reijven. Provides an overview of fundamental/foundational content and then goes on to translate the information to more clinically-oriented perspectives Highlights the benefit of normal pathophysiological response to stress and the misunderstandings surrounding the treatment of this response Explains how treatment should be adapted to support the inflammatory response and how to treat its inflammatory cause Includes case studies and slides
