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Search Results: 1 - 10 of 435659 matches for " G. J. Lieschke "
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Hydrogen Peroxide in Inflammation: Messenger, Guide, and Assassin
C. Wittmann,P. Chockley,S. K. Singh,L. Pase,G. J. Lieschke,C. Grabher
Advances in Hematology , 2012, DOI: 10.1155/2012/541471
Abstract: Starting as a model for developmental genetics, embryology, and organogenesis, the zebrafish has become increasingly popular as a model organism for numerous areas of biology and biomedicine over the last decades. Within haematology, this includes studies on blood cell development and function and the intricate regulatory mechanisms within vertebrate immunity. Here, we review recent studies on the immediate mechanisms mounting an inflammatory response by in vivo analyses using the zebrafish. These recently revealed novel roles of the reactive oxygen species hydrogen peroxide that have changed our view on the initiation of a granulocytic inflammatory response. 1. Introduction The innate immune system comprises the cells and mechanisms that defend the host from infection by other organisms or damage to tissue integrity, in a nonspecific manner. This means that the cells of the innate system recognise and respond to pathogens and trauma in a generic way, but unlike the adaptive immune system, it does not confer long-lasting or protective immunity to the host. The innate immune system provides an immediate defence. A typical vertebrate immune response depends on the orchestrated motility and activity of various haematopoietic compartments and their interactions that ultimately control the magnitude of the response [1–3]. Inflammation is one of the first responses of the immune system to infection or irritation. Stimulated by factors released from injured cells, it serves to establish a physical barrier against the spread of infection. This further promotes healing of any damaged tissue following the clearance of pathogens or cell debris. Molecules produced during inflammation sensitise pain receptors, cause localised vasodilatation of blood vessels, and attract phagocytes, especially neutrophils and macrophages, which then trigger other parts of the immune system. Failure to initiate a response allows uncontrolled proliferation of invading microorganisms and severe tissue damage that may become fatal. Failure to resolve an immune response can also cause severe tissue damage, due to persistent degranulation, and may lead to chronic inflammation, which ceases to be beneficial to the host. Overall, inflammation is now recognised as a central feature of prevalent pathologies, such as atherosclerosis, cancer, asthma, thyroiditis, inflammatory bowel disease, autoimmune disease, as well as Alzheimer’s and Parkinson’s disease [4–6]. Hence, the regulation of an inflammatory response is an active field of research. New players or novel functions of old players
Mediator Subunit 12 Is Required for Neutrophil Development in Zebrafish
Maria-Cristina Keightley, Judith E. Layton, John W. Hayman, Joan K. Heath, Graham J. Lieschke
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0023845
Abstract: Hematopoiesis requires the spatiotemporal organization of regulatory factors to successfully orchestrate diverse lineage specificity from stem and progenitor cells. Med12 is a regulatory component of the large Mediator complex that enables contact between the general RNA polymerase II transcriptional machinery and enhancer bound regulatory factors. We have identified a new zebrafish med12 allele, syr, with a single missense mutation causing a valine to aspartic acid change at position 1046. Syr shows defects in hematopoiesis, which predominantly affect the myeloid lineage. Syr has identified a hematopoietic cell-specific requirement for Med12, suggesting a new role for this transcriptional regulator.
Nerve Growth Factor Stimulates Cardiac Regeneration via Cardiomyocyte Proliferation in Experimental Heart Failure
Nicholas T. Lam, Peter D. Currie, Graham J. Lieschke, Nadia A. Rosenthal, David M. Kaye
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0053210
Abstract: Although the adult heart likely retains some regenerative capacity, heart failure (HF) typically remains a progressive disorder. We hypothesise that alterations in the local environment contribute to the failure of regeneration in HF. Previously we showed that nerve growth factor (NGF) is deficient in the failing heart and here we hypothesise that diminished NGF limits the cardiac regenerative response in HF. The capacity of NGF to augment cardiac regeneration was tested in a zebrafish model of HF. Cardiac injury with a HF phenotype was induced in zebrafish larvae at 72 hours post fertilization (hpf) by exposure to aristolochic acid (AA, 2.5 μM, 72–75 hpf). By 168 hpf, AA induced HF and death in 37.5% and 20.8% of larvae respectively (p<0.001). NGF mRNA expression was reduced by 42% (p<0.05). The addition of NGF (50 ng/ml) after exposure to AA reduced the incidence of HF by 50% (p<0.01) and death by 65% (p<0.01). Mechanistically, AA mediated HF was characterised by reduced cardiomyocyte proliferation as reflected by a 6.4 fold decrease in BrdU+ cardiomyocytes (p<0.01) together with features of apoptosis and loss of cardiomyocytes. Following AA exposure, NGF increased the abundance of BrdU+ cardiomyocytes in the heart by 4.8 fold (p<0.05), and this was accompanied by a concomitant significant increase in cardiomyocyte numbers. The proliferative effect of NGF on cardiomyocytes was not associated with an anti-apoptotic effect. Taken together the study suggests that NGF stimulates a regenerative response in the failing zebrafish heart, mediated by stimulation of cardiomyocyte proliferation.
PhagoSight: An Open-Source MATLAB? Package for the Analysis of Fluorescent Neutrophil and Macrophage Migration in a Zebrafish Model
Katherine M. Henry, Luke Pase, Carlos Fernando Ramos-Lopez, Graham J. Lieschke, Stephen A. Renshaw, Constantino Carlos Reyes-Aldasoro
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0072636
Abstract: Neutrophil migration in zebrafish larvae is increasingly used as a model to study the response of these leukocytes to different determinants of the cellular inflammatory response. However, it remains challenging to extract comprehensive information describing the behaviour of neutrophils from the multi-dimensional data sets acquired with widefield or confocal microscopes. Here, we describe PhagoSight, an open-source software package for the segmentation, tracking and visualisation of migrating phagocytes in three dimensions. The algorithms in PhagoSight extract a large number of measurements that summarise the behaviour of neutrophils, but that could potentially be applied to any moving fluorescent cells. To derive a useful panel of variables quantifying aspects of neutrophil migratory behaviour, and to demonstrate the utility of PhagoSight, we evaluated changes in the volume of migrating neutrophils. Cell volume increased as neutrophils migrated towards the wound region of injured zebrafish. PhagoSight is openly available as MATLAB? m-files under the GNU General Public License. Synthetic data sets and a comprehensive user manual are available from http://www.phagosight.org.
Real-Time Whole-Body Visualization of Chikungunya Virus Infection and Host Interferon Response in Zebrafish
Nuno Palha,Florence Guivel-Benhassine,Valérie Briolat,Georges Lutfalla,Marion Sourisseau,Felix Ellett,Chieh-Huei Wang,Graham J. Lieschke,Philippe Herbomel,Olivier Schwartz,Jean-Pierre Levraud
PLOS Pathogens , 2013, DOI: 10.1371/journal.ppat.1003619
Abstract: Chikungunya Virus (CHIKV), a re-emerging arbovirus that may cause severe disease, constitutes an important public health problem. Herein we describe a novel CHIKV infection model in zebrafish, where viral spread was live-imaged in the whole body up to cellular resolution. Infected cells emerged in various organs in one principal wave with a median appearance time of ~14 hours post infection. Timing of infected cell death was organ dependent, leading to a shift of CHIKV localization towards the brain. As in mammals, CHIKV infection triggered a strong type-I interferon (IFN) response, critical for survival. IFN was mainly expressed by neutrophils and hepatocytes. Cell type specific ablation experiments further demonstrated that neutrophils play a crucial, unexpected role in CHIKV containment. Altogether, our results show that the zebrafish represents a novel valuable model to dynamically visualize replication, pathogenesis and host responses to a human virus.
Autophagy Induction Is a Tor- and Tp53-Independent Cell Survival Response in a Zebrafish Model of Disrupted Ribosome Biogenesis
Yeliz Boglev,Andrew P. Badrock,Andrew J. Trotter,Qian Du,Elsbeth J. Richardson,Adam C. Parslow,Sebastian J. Markmiller,Nathan E. Hall,Tanya A. de Jong-Curtain,Annie Y. Ng,Heather Verkade,Elke A. Ober,Holly A. Field,Donghun Shin,Chong H. Shin,Katherine M. Hannan,Ross D. Hannan,Richard B. Pearson,Seok-Hyung Kim,Kevin C. Ess,Graham J. Lieschke,Didier Y. R. Stainier,Joan K. Heath
PLOS Genetics , 2013, DOI: 10.1371/journal.pgen.1003279
Abstract: Ribosome biogenesis underpins cell growth and division. Disruptions in ribosome biogenesis and translation initiation are deleterious to development and underlie a spectrum of diseases known collectively as ribosomopathies. Here, we describe a novel zebrafish mutant, titania (ttis450), which harbours a recessive lethal mutation in pwp2h, a gene encoding a protein component of the small subunit processome. The biochemical impacts of this lesion are decreased production of mature 18S rRNA molecules, activation of Tp53, and impaired ribosome biogenesis. In ttis450, the growth of the endodermal organs, eyes, brain, and craniofacial structures is severely arrested and autophagy is up-regulated, allowing intestinal epithelial cells to evade cell death. Inhibiting autophagy in ttis450 larvae markedly reduces their lifespan. Somewhat surprisingly, autophagy induction in ttis450 larvae is independent of the state of the Tor pathway and proceeds unabated in Tp53-mutant larvae. These data demonstrate that autophagy is a survival mechanism invoked in response to ribosomal stress. This response may be of relevance to therapeutic strategies aimed at killing cancer cells by targeting ribosome biogenesis. In certain contexts, these treatments may promote autophagy and contribute to cancer cells evading cell death.
Conditioning Strategies Limit Cellular Injury?  [PDF]
J. G. Kingma
World Journal of Cardiovascular Diseases (WJCD) , 2014, DOI: 10.4236/wjcd.2014.411065
Abstract: Evaluation of multiorgan protection strategies against ischemic injury in humans is essential to improve quality of life and reduce mortality. Over the past 40 years a host of pharmacologic and non-pharmacologic interventions have been evaluated with the aim of limiting cell damage produced by ischemia-reperfusion injury. Different conditioning strategies, such as remote conditioning, are documented to mitigate ischemic injury in animal and human studies and may have remarkable clinical promise. However, successful clinical application of these interventions remains questionable since protection is known to be compromised in humans with comorbidities either with or without medications. Regardless, ongoing studies continue to examine the underlying mechanisms involved in this endogenous cytoprotective phenomenon to further its successful implementation in the clinical setting. In this review, we examine recent findings in support of remote conditioning stratagems for organ protection and their relevance for translation to clinical use.
Myocardial Infarction: An Overview of STEMI and NSTEMI Physiopathology and Treatment  [PDF]
J. G. Kingma
World Journal of Cardiovascular Diseases (WJCD) , 2018, DOI: 10.4236/wjcd.2018.811049
Abstract: Patients with myocardial infarction resulting from acute coronary syndrome are classified by electrocardiographic presentation: 1-acute ST-segment elevation myocardial infarction (STEMI) or 2-non-ST-segment elevation myocardial infarction (NSTEMI). Prompt reperfusion of an infarct-related artery by percutaneous coronary interventions provides some relief of symptoms; long-term prognosis appears to be worse in STEMI compared to NSTEMI patients but clinical findings remain controversial. Reduced myocardial perfusion to the infarct area, caused in part by microvascular obstruction, is a privileged target for diverse pharmacologic or non-pharmacologic interventions (or combinations thereof) to improve clinical outcomes. To date, benefits of both pharmacologic and non-pharmacologic strategies to either limit microvascular obstruction and myocardial injury or improve myocardial perfusion are inconsistent. This review focuses on the physiopathological aspects of myocardial infarction in relation to development of STEMI/NSTEMI and on potential cardioprotective strategies.
A Photonic Model of the Big Bang  [PDF]
J. G. Lartigue
Journal of Modern Physics (JMP) , 2018, DOI: 10.4236/jmp.2018.914157
Abstract: There are two main theories about the origin of the Universe that show similitude with the Genesis writings, though in different verses: the Big Bang1 and the eternal Universe2 (an eventual quantum fluctuation). However, it is possible to partially include the quantum theory in the Big Bang thanks to the nature of photons, to obtain a simple model. It is assumed as the origin of the Universe (space, time, matter and physical laws). A subsequent enormous expansion has been explained by a supposed brief Inflation period, followed up today by a constant adiabatic expansion acceleration. This paper assumes that the Universe is the total Space which contains the Physical Universe covered by an external, empty Space, both expanding at a constant Hubble acceleration ΓH [1]. A Big Bang design is intended by a deduction of the energy and number of primeval photons, from the present CMB value; they would have reacted whether to generate the Physical Universe or to decay till the CMB level. It follows an approach to the Universe expansion work, based on the Hubble field (VH) as well as on Thermo-dynamics. They are calculated: the time and angular momentum required for the Physical Universe to reach the maximum internal velocity c as well as, simultaneously, a c tangential velocity. The Universe luminosity at different periods and the adequate expressions of parameters (Ω, q, k) are revised. It is proposed a modification in the equation of the H(t) parameter and the Ho value. The operator of convective derivative is applied to obtain an equation of continuity for the photonic energy; an adiabatic Jacobian gives similar results. This essay differs from others based on black box radiation, since the Universe has no walls and the photons energy decays continuously.
Multi-Cultural Dynamics on Social Networks under External Random Perturbations  [PDF]
J. Chandra, G. S. Ladde
Int'l J. of Communications, Network and System Sciences (IJCNS) , 2014, DOI: 10.4236/ijcns.2014.76020

This work deals with the development of multi-cultural network-centric dynamic models under the influence of personal intra- and inter-members, as well as community. Each individual member of a society is influenced by her/his interactions with fellow members of the family, neighborhood, region and the universe. The behavior of such complex and highly interacting social networks is characterized by stochastic interconnected dynamical systems. The primary goal is on laying down an investigation of both qualitative and quantitative properties of this network dynamical system. In particular, we would like to determine the regions of conflicts and coexietence as well as to establish the cohesion and stability of emerging states. This is achieved by employing the method of system of differential inequalities and comparison theorems in the context of the energy function. The developed energy function method provides estimates for regions of conflict and cooperation. Moreover, the method also provides sufficient conditions for the community cohesion and stability in a systematic way.

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