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Search Results: 1 - 10 of 216464 matches for " Jennifer L. Taylor-Cousar "
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Potential of anti-inflammatory treatment for cystic fibrosis lung disease
Jennifer L Taylor-Cousar, Kelsey A Von Kessel, Robert Young, et al
Journal of Inflammation Research , 2010, DOI: http://dx.doi.org/10.2147/JIR.S8875
Abstract: tential of anti-inflammatory treatment for cystic fibrosis lung disease Review (5439) Total Article Views Authors: Jennifer L Taylor-Cousar, Kelsey A Von Kessel, Robert Young, et al Published Date August 2010 Volume 2010:3 Pages 61 - 74 DOI: http://dx.doi.org/10.2147/JIR.S8875 Jennifer L Taylor-Cousar1,2, Kelsey A Von Kessel2, Robert Young1, David P Nichols1,2 1Department of Medicine, National Jewish Health, Denver, Colorado, USA; 2Department of Pediatrics, National Jewish Health, Denver, Colorado, USA Abstract: Cystic fibrosis (CF) is the most common life-shortening genetic disorder in -Caucasians. With improved diagnosis and treatment, survival has steadily increased. -Unfortunately, the overwhelming majority of patients still die from respiratory failure caused by structural damage resulting from airway obstruction, recurrent infection, and inflammation. Here, we discuss the role of inflammation and the development of anti-inflammatory therapies to treat CF lung disease. The inflammatory host response is the least addressed component of CF airway disease at this time. Current challenges in both preclinical and clinical investigation make the identification of suitable anti-inflammatory drugs more difficult. Despite this, many researchers are making significant progress toward this goal and the CF research community has reason to believe that new therapies will emerge from these efforts.
Potential of anti-inflammatory treatment for cystic fibrosis lung disease
Jennifer L Taylor-Cousar,Kelsey A Von Kessel,Robert Young,et al
Journal of Inflammation Research , 2010,
Abstract: Jennifer L Taylor-Cousar1,2, Kelsey A Von Kessel2, Robert Young1, David P Nichols1,21Department of Medicine, National Jewish Health, Denver, Colorado, USA; 2Department of Pediatrics, National Jewish Health, Denver, Colorado, USAAbstract: Cystic fibrosis (CF) is the most common life-shortening genetic disorder in -Caucasians. With improved diagnosis and treatment, survival has steadily increased. -Unfortunately, the overwhelming majority of patients still die from respiratory failure caused by structural damage resulting from airway obstruction, recurrent infection, and inflammation. Here, we discuss the role of inflammation and the development of anti-inflammatory therapies to treat CF lung disease. The inflammatory host response is the least addressed component of CF airway disease at this time. Current challenges in both preclinical and clinical investigation make the identification of suitable anti-inflammatory drugs more difficult. Despite this, many researchers are making significant progress toward this goal and the CF research community has reason to believe that new therapies will emerge from these efforts.Keywords: therapy, cystic fibrosis, survival, inflammation
Histo-Blood Group Gene Polymorphisms as Potential Genetic Modifiers of Infection and Cystic Fibrosis Lung Disease Severity
Jennifer L. Taylor-Cousar, Maimoona A. Zariwala, Lauranell H. Burch, Rhonda G. Pace, Mitchell L. Drumm, Hollin Calloway, Haiying Fan, Brent W. Weston, Fred A. Wright, Michael R. Knowles, for the Gene Modifier Study Group
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0004270
Abstract: Background The pulmonary phenotype in cystic fibrosis (CF) is variable; thus, environmental and genetic factors likely contribute to clinical heterogeneity. We hypothesized that genetically determined ABO histo-blood group antigen (ABH) differences in glycosylation may lead to differences in microbial binding by airway mucus, and thus predispose to early lung infection and more severe lung disease in a subset of patients with CF. Methods and Principal Findings Clinical information and DNA was collected on >800 patients with the ΔF508/ΔF508 genotype. Patients in the most severe and mildest quartiles for lung phenotype were enrolled. Blood samples underwent lymphocyte transformation and DNA extraction using standard methods. PCR and sequencing were performed using standard techniques to identify the 9 SNPs required to determine ABO blood type, and to identify the four SNPs that account for 90–95% of Lewis status in Caucasians. Allele identification of the one nonsynonymous SNP in FUT2 that accounts for >95% of the incidence of nonsecretor phenotype in Caucasians was completed using an ABI Taqman assay. The overall prevalence of ABO types, and of FUT2 (secretor) and FUT 3 (Lewis) alleles was consistent with that found in the Caucasian population. There was no difference in distribution of ABH type in the severe versus mild patients, or the age of onset of Pseudomonas aeruginosa infection in the severe or mild groups. Multivariate analyses of other clinical phenotypes, including gender, asthma, and meconium ileus demonstrated no differences between groups based on ABH type. Conclusions and Significance Polymorphisms in the genes encoding ABO blood type, secretor or Lewis genotypes were not shown to associate with severity of CF lung disease, or age of onset of P. aeruginosa infection, nor was there any association with other clinical phenotypes in a group of 808 patients homozygous for the ΔF508 mutation.
Neutrophil Extracellular Trap (NET)-Mediated Killing of Pseudomonas aeruginosa: Evidence of Acquired Resistance within the CF Airway, Independent of CFTR
Robert L. Young, Kenneth C. Malcolm, Jennifer E. Kret, Silvia M. Caceres, Katie R. Poch, David P. Nichols, Jennifer L. Taylor-Cousar, Milene T. Saavedra, Scott H. Randell, Michael L. Vasil, Jane L. Burns, Samuel M. Moskowitz, Jerry A. Nick
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0023637
Abstract: The inability of neutrophils to eradicate Pseudomonas aeruginosa within the cystic fibrosis (CF) airway eventually results in chronic infection by the bacteria in nearly 80 percent of patients. Phagocytic killing of P. aeruginosa by CF neutrophils is impaired due to decreased cystic fibrosis transmembrane conductance regulator (CFTR) function and virulence factors acquired by the bacteria. Recently, neutrophil extracellular traps (NETs), extracellular structures composed of neutrophil chromatin complexed with granule contents, were identified as an alternative mechanism of pathogen killing. The hypothesis that NET-mediated killing of P. aeruginosa is impaired in the context of the CF airway was tested. P. aeruginosa induced NET formation by neutrophils from healthy donors in a bacterial density dependent fashion. When maintained in suspension through continuous rotation, P. aeruginosa became physically associated with NETs. Under these conditions, NETs were the predominant mechanism of killing, across a wide range of bacterial densities. Peripheral blood neutrophils isolated from CF patients demonstrated no impairment in NET formation or function against P. aeruginosa. However, isogenic clinical isolates of P. aeruginosa obtained from CF patients early and later in the course of infection demonstrated an acquired capacity to withstand NET-mediated killing in 8 of 9 isolates tested. This resistance correlated with development of the mucoid phenotype, but was not a direct result of the excess alginate production that is characteristic of mucoidy. Together, these results demonstrate that neutrophils can kill P. aeruginosa via NETs, and in vitro this response is most effective under non-stationary conditions with a low ratio of bacteria to neutrophils. NET-mediated killing is independent of CFTR function or bacterial opsonization. Failure of this response in the context of the CF airway may occur, in part, due to an acquired resistance against NET-mediated killing by CF strains of P. aeruginosa.
Therapeutic Use of Dendritic Cells to Promote the Extranodal Priming of Anti-Tumor Immunity
Jennifer L. Taylor,Walter J. Storkus
Frontiers in Immunology , 2013, DOI: 10.3389/fimmu.2013.00388
Abstract: Ectopic lymphoid tissue, also known as tertiary lymphoid organs (TLO) develop adaptively within sites of chronic tissue inflammation, thereby allowing the host to efficiently crossprime specific immune effector cells within sites of disease. Recent evidence suggests that the presence of TLO in the tumor microenvironment (TME) predicts better overall survival. We will discuss the relevance of extranodal T cell priming within the TME as a means to effectively promote anti-tumor immunity and the strategic use of dendritic cell (DC)-based therapies to reinforce this clinically preferred process in the cancer-bearing host.
Interactions along an Entanglement Cut in 2+1D Abelian Topological Phases
Jennifer Cano,Taylor L. Hughes,Michael Mulligan
Physics , 2014, DOI: 10.1103/PhysRevB.92.075104
Abstract: A given fractional quantum Hall state may admit multiple, distinct edge phases on its boundary. We explore the implications that multiple edge phases have for the entanglement spectrum and entropy of a given bulk state. We describe the precise manner in which the entanglement spectrum depends upon local (tunneling) interactions along an entanglement cut and throughout the bulk. The sensitivity to local conditions near the entanglement cut appears not only in gross features of the spectrum, but can also manifest itself in an additive, positive constant correction to the topological entanglement entropy, i.e., it increases its magnitude. A natural interpretation for this result is that the tunneling interactions across an entanglement cut can function as a barrier to certain types of quasiparticle transport across the cut, thereby, lowering the total entanglement between the two regions.
Disrupting Ovarian Cancer Metastatic Colonization: Insights from Metastasis Suppressor Studies
Shaheena Khan,Jennifer L. Taylor,Carrie W. Rinker-Schaeffer
Journal of Oncology , 2010, DOI: 10.1155/2010/286925
Abstract: Ovarian cancer affects approximately 25,000 women in the United States each year and remains one of the most lethal female malignancies. A standard approach to therapy is surgical cytoreduction, after which the remaining microscopic residual disease is treated with chemotherapy. The vast majority of patients have disease recurrence, underscoring the crucial need for approaches to control the regrowth, or colonization, of tissues after local treatment. Improved therapies require mechanistic information about the process of metastatic colonization, the final step in metastasis, in which cancer cells undergo progressive growth at secondary sites. Studies of metastasis suppressors are providing insights into events controlling metastatic colonization. This paper reviews our laboratory's approach to the identification, characterization, and functional testing of the JNKK1/MKK4 metastasis suppressor in ovarian cancer metastatic colonization. Specifically, we demonstrate that interaction of ovarian caner cells with the omental microenvironment activates JNKK1/MKK4 resulting in decreased proliferation without affecting apoptosis. The potential role of the omental microenvironment, specifically milky spot structures, is also described. It is our goal to provide this work as a usable paradigm that will enable others to study metastasis suppressors in clinical and experimental ovarian cancer metastases. 1. Introduction Management of metastatic ovarian cancer continues to be a critical clinical problem. Ovarian cancer affects close to 25,000 women yearly [1] and most patients have extensive metastatic disease at the time of diagnosis.Ovarian cancer metastasis is thought to result from exfoliation of tumor cells from the ovary and/or direct extension onto the peritoneal surfaces, the omentum, and the surface of organs such as the liver and bowel. A standard approach to therapy is to surgically remove surgically as much of the tumor(s) as possible, a process known as surgical cytoreduction. This technique, which leaves only microscopic residual disease, is used in conjunction with chemotherapy. Unfortunately, more than 80% of patients have cancer regrowth. These dismal statistics show the need for improved understanding of the process of metastatic colonization, the final step in metastasis, in which cancer cells undergo progressive growth at secondary sites [2, 3] (see Figure 1). While invasion and adhesion have been well studied, mechanisms regulating metastatic colonization are largely unknown. Studies of metastasis suppressors are providing insights into events
Marine Reserves and Reproductive Biomass: A Case Study of a Heavily Targeted Reef Fish
Brett M. Taylor, Jennifer L. McIlwain, Alexander M. Kerr
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0039599
Abstract: Recruitment overfishing (the reduction of a spawning stock past a point at which the stock can no longer replenish itself) is a common problem which can lead to a rapid and irreversible fishery collapse. Averting this disaster requires maintaining a sufficient spawning population to buffer stochastic fluctuations in recruitment of heavily harvested stocks. Optimal strategies for managing spawner biomass are well developed for temperate systems, yet remain uncertain for tropical fisheries, where the danger of collapse from recruitment overfishing looms largest. In this study, we explored empirically and through modeling, the role of marine reserves in maximizing spawner biomass of a heavily exploited reef fish, Lethrinus harak around Guam, Micronesia. On average, spawner biomass was 16 times higher inside the reserves compared with adjacent fished sites. Adult density and habitat-specific mean fish size were also significantly greater. We used these data in an age-structured population model to explore the effect of several management scenarios on L. harak demography. Under minimum-size limits, unlimited extraction and all rotational-closure scenarios, the model predicts that preferential mortality of larger and older fish prompt dramatic declines in spawner biomass and the proportion of male fish, as well as considerable declines in total abundance. For rotational closures this occurred because of the mismatch between the scales of recovery and extraction. Our results highlight how alternative management scenarios fall short in comparison to marine reserves in preserving reproductively viable fish populations on coral reefs.
Alert but less alarmed: a pooled analysis of terrorism threat perception in Australia
Garry Stevens, Kingsley Agho, Melanie Taylor, Alison L Jones, Jennifer Jacobs, Margo Barr, Beverley Raphael
BMC Public Health , 2011, DOI: 10.1186/1471-2458-11-797
Abstract: Representative samples of New South Wales (NSW) adults completed terrorism perception questions as part of computer assisted telephone interviews (CATI) in 2007 (N = 2081) and 2010 (N = 2038). Responses were weighted against the NSW population. Data sets from the two surveys were pooled and multivariate multilevel analyses conducted to identify health and socio-demographic factors associated with higher perceived risk of terrorism and evacuation response intentions, and to examine changes over time.In comparison with 2007, Australians in 2010 were significantly more likely to believe that a terrorist attack would occur in Australia (Adjusted Odd Ratios (AOR) = 1.24, 95%CI:1.06-1.45) but felt less concerned that they would be directly affected by such an incident (AOR = 0.65, 95%CI:0.55-0.75). Higher perceived risk of terrorism and related changes in living were associated with middle age, female gender, lower education and higher reported psychological distress. Australians of migrant background reported significantly lower likelihood of terrorism (AOR = 0.52, 95%CI:0.39-0.70) but significantly higher concern that they would be personally affected by such an incident (AOR = 1.57, 95%CI:1.21-2.04) and having made changes in the way they live due to this threat (AOR = 2.47, 95%CI:1.88-3.25). Willingness to evacuate homes and public places in response to potential incidents increased significantly between 2007 and 2010 (AOR = 1.53, 95%CI:1.33-1.76).While an increased proportion of Australians believe that the national threat of terrorism remains high, concern about being personally affected has moderated and may reflect habituation to this threat. Key sub-groups remain disproportionately concerned, notably those with lower education and migrant groups. The dissonance observed in findings relating to Australians of migrant background appears to reflect wider socio-cultural concerns associated with this issue. Disparities in community concerns regarding terrorism-related
Characterization of a molecular switch system that regulates gene expression in mammalian cells through a small molecule
Jennifer L Taylor, Priyanka Rohatgi, H Trent Spencer, Donald F Doyle, Bahareh Azizi
BMC Biotechnology , 2010, DOI: 10.1186/1472-6750-10-15
Abstract: This work focuses on characterizing a molecular switch system that quantitatively controls transgene expression. This system is composed of an orthogonal ligand/nuclear receptor pair, LG335 and GRQCIMFI, along with an artificial promoter controlling expression of a target transgene. GRQCIMFI is composed of the fusion of the DNA binding domain of the yeast transcription factor, Gal4, and a retinoid × receptor variant. The variant consists of the following mutations: Q275C, I310M, and F313I in the ligand binding domain. When introduced into mammalian cell culture, the switch shows luciferase activity at concentrations as low as 100 nM of LG335 with a 6.3 ± 1.7-fold induction ratio. The developed one-component system activates transgene expression when introduced transiently or virally.We have successfully shown that this system can induce tightly controlled transgene expression and can be used for transient transfections or retroviral transductions in mammalian cell culture. Further characterization is needed for gene therapy applications.Gene regulation systems are important research tools for studying gene function and can provide numerous benefits for clinical applications. Several systems have been designed that place a target transgene under the control of an engineered transcription factor that is activated in the presence of an exogenous ligand [1]. These systems have been successfully used to control expression of a target transgene in a cellular environment with high expression levels in response to an extensive range of ligand concentrations [2]. To date, several research groups have used these systems to control transgene expression in both cell culture as well as animal models. Some of the most commonly used examples include the progesterone receptor (PR)/mifepristone (RU486) inducible system [3], the tetracycline inducible system [4], and the ecdysone-responsive regulation system [5].The progesterone receptor (PR) inducible system, also known as GeneSwitc
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