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Search Results: 1 - 10 of 401320 matches for " Treuting Piper M "
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Practical pathology of aging mice
Christina Pettan-Brewer,Piper M. M. Treuting
Pathobiology of Aging & Age-related Diseases , 2011, DOI: 10.3402/pba.v1i0.7202
Abstract: Old mice will have a subset of lesions as part of the progressive decline in organ function that defines aging. External and palpable lesions will be noted by the research, husbandry, or veterinary staff during testing, cage changing, or physical exams. While these readily observable lesions may cause alarm, not all cause undue distress or are life-threatening. In aging research, mice are maintained until near end of life that, depending on strain and genetic manipulation, can be upwards of 33 months. Aging research has unique welfare issues related to age-related decline, debilitation, fragility, and associated pain of chronic diseases. An effective aging research program includes the collaboration and education of the research, husbandry, and veterinary staff, and of the members of the institution animal care and use committee. This collaborative effort is critical to humanely maintaining older mice and preventing excessive censorship due to non-lethal diseases. Part of the educational process is becoming familiar with how old mice appear clinically, at necropsy and histopathologically. This baseline knowledge is important in making the determination of humane end points, defining health span, contributing causes of death and effects of interventions. The goal of this paper is to introduce investigators to age-associated diseases and lesion patterns in mice from clinical presentation to pathologic assessment. To do so, we present and illustrate the common clinical appearances, necropsy and histopathological lesions seen in subsets of the aging colonies maintained at the University of Washington.
Interleukin-7 receptor blockade suppresses adaptive and innate inflammatory responses in experimental colitis
Willis Cynthia R,Seamons Audrey,Maxwell Joe,Treuting Piper M
Journal of Inflammation , 2012, DOI: 10.1186/1476-9255-9-39
Abstract: Background Interleukin-7 (IL-7) acts primarily on T cells to promote their differentiation, survival, and homeostasis. Under disease conditions, IL-7 mediates inflammation through several mechanisms and cell types. In humans, IL-7 and its receptor (IL-7R) are increased in diseases characterized by inflammation such as atherosclerosis, rheumatoid arthritis, psoriasis, multiple sclerosis, and inflammatory bowel disease. In mice, overexpression of IL-7 results in chronic colitis, and T-cell adoptive transfer studies suggest that memory T cells expressing high amounts of IL-7R drive colitis and are maintained and expanded with IL-7. The studies presented here were undertaken to better understand the contribution of IL-7R in inflammatory bowel disease in which colitis was induced with a bacterial trigger rather than with adoptive transfer. Methods We examined the contribution of IL-7R on inflammation and disease development in two models of experimental colitis: Helicobacter bilis (Hb)-induced colitis in immune-sufficient Mdr1a / mice and in T- and B-cell-deficient Rag2 / mice. We used pharmacological blockade of IL-7R to understand the mechanisms involved in IL-7R-mediated inflammatory bowel disease by analyzing immune cell profiles, circulating and colon proteins, and colon gene expression. Results Treatment of mice with an anti-IL-7R antibody was effective in reducing colitis in Hb-infected Mdr1a / mice by reducing T-cell numbers as well as T-cell function. Down regulation of the innate immune response was also detected in Hb-infected Mdr1a / mice treated with an anti-IL-7R antibody. In Rag2 / mice where colitis was triggered by Hb-infection, treatment with an anti-IL-7R antibody controlled innate inflammatory responses by reducing macrophage and dendritic cell numbers and their activity. Conclusions Results from our studies showed that inhibition of IL-7R successfully ameliorated inflammation and disease development in Hb-infected mice by controlling the expansion of multiple leukocyte populations, as well as the activity of these immune cells. Our findings demonstrate an important function of IL-7R-driven immunity in experimental colitis and indicate that the therapeutic efficacy of IL-7R blockade involves affecting both adaptive and innate immunity.
Characterization of Dextran Sodium Sulfate-Induced Inflammation and Colonic Tumorigenesis in Smad3?/? Mice with Dysregulated TGFβ
Audrey Seamons, Piper M. Treuting, Thea Brabb, Lillian Maggio-Price
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0079182
Abstract: There are few mouse models that adequately mimic large bowel cancer in humans or the gastrointestinal inflammation which frequently precedes it. Dextran sodium sulphate (DSS)-induces colitis in many animal models and has been used in combination with the carcinogen azoxymethane (AOM) to induce cancer in mice. Smad3?/? mice are deficient in the transforming growth factor beta (TGFβ) signaling molecule, SMAD3, resulting in dysregulation of the cellular pathway most commonly affected in human colorectal cancer, and develop inflammation-associated colon cancer. Previous studies have shown a requirement for a bacterial trigger for the colitis and colon cancer phenotype in Smad3?/? mice. Studies presented here in Smad3?/? mice detail disease induction with DSS, without the use of AOM, and show a) Smad3?/? mice develop a spectrum of lesions ranging from acute and chronic colitis, crypt herniation, repair, dysplasia, adenomatous polyps, disseminated peritoneal adenomucinosis, adenocarcinoma, mucinous adenocarcinoma (MAC) and squamous metaplasia; b) the colon lesions have variable galactin-3 (Mac2) staining c) increased DSS concentration and duration of exposure leads to increased severity of colonic lesions; d) heterozygosity of SMAD3 does not confer increased susceptibility to DSS-induced disease and e) disease is partially controlled by the presence of T and B cells as Smad3?/?Rag2?/? double knock out (DKO) mice develop a more severe disease phenotype. DSS-induced disease in Smad3?/? mice may be a useful animal model to study not only inflammation-driven MAC but other human diseases such as colitis cystica profunda (CCP) and pseudomyxomatous peritonei (PMP).
IL-1β Signaling Promotes CNS-Intrinsic Immune Control of West Nile Virus Infection
Hilario J. Ramos,Marion C. Lanteri,Gabriele Blahnik,Amina Negash,Mehul S. Suthar,Margaret M. Brassil,Khushbu Sodhi,Piper M. Treuting,Michael P. Busch,Philip J. Norris,Michael Gale Jr.
PLOS Pathogens , 2012, DOI: 10.1371/journal.ppat.1003039
Abstract: West Nile virus (WNV) is an emerging flavivirus capable of infecting the central nervous system (CNS) and mediating neuronal cell death and tissue destruction. The processes that promote inflammation and encephalitis within the CNS are important for control of WNV disease but, how inflammatory signaling pathways operate to control CNS infection is not defined. Here, we identify IL-1β signaling and the NLRP3 inflammasome as key host restriction factors involved in viral control and CNS disease associated with WNV infection. Individuals presenting with acute WNV infection displayed elevated levels of IL-1β in their plasma over the course of infection, suggesting a role for IL-1β in WNV immunity. Indeed, we found that in a mouse model of infection, WNV induced the acute production of IL-1β in vivo, and that animals lacking the IL-1 receptor or components involved in inflammasome signaling complex exhibited increased susceptibility to WNV pathogenesis. This outcome associated with increased accumulation of virus within the CNS but not peripheral tissues and was further associated with altered kinetics and magnitude of inflammation, reduced quality of the effector CD8+ T cell response and reduced anti-viral activity within the CNS. Importantly, we found that WNV infection triggers production of IL-1β from cortical neurons. Furthermore, we found that IL-1β signaling synergizes with type I IFN to suppress WNV replication in neurons, thus implicating antiviral activity of IL-1β within neurons and control of virus replication within the CNS. Our studies thus define the NLRP3 inflammasome pathway and IL-1β signaling as key features controlling WNV infection and immunity in the CNS, and reveal a novel role for IL-1β in antiviral action that restricts virus replication in neurons.
A Consistency Condition for the Double Series Approximation Method
M. S. Piper
Physics , 1996, DOI: 10.1088/0264-9381/14/3/019
Abstract: The double series approximation method of Bonnor is a means for examining the gravitational radiation from an axisymmetric isolated source that undergoes a finite period of oscillation. It involves an expansion of the metric as a double Taylor series. Here we examine the integration procedure that is used to form an algorithmic solution to the field equations and point out the possibility of the expansion method breaking down and predicting a singularity along the axis of symmetry. We derive a condition on the solutions obtained by the double series method that must be satisfied to avoid this singularity. We then consider a source with only a quadrupole moment and verify that to fourth order in each of the expansion parameters, this condition is satisfied. This is a reassuring test of the consistency of the expansion procedure. We do, however, find that the imposition of this condition makes a physical interpretation of any but the lowest order solutions very difficult. The most obvious decomposition of the solution into a series of independent physical effects is shown not to be valid.
Disruption of Protein Kinase A in Mice Enhances Healthy Aging
Linda C. Enns, John F. Morton, Piper R. Treuting, Mary J. Emond, Norman S. Wolf, G. S. McKnight, Peter S. Rabinovitch, Warren C. Ladiges
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0005963
Abstract: Mutations that cause a reduction in protein kinase A (PKA) activity have been shown to extend lifespan in yeast. Loss of function of mammalian RIIβ, a regulatory subunit of PKA expressed in brain and adipose tissue, results in mice that are lean and insulin sensitive. It was therefore hypothesized that RIIB null (RIIβ?/?) mice would express anti-aging phenotypes. We conducted lifespan studies using 40 mutant and 40 wild type (WT) littermates of equal gender numbers and found that both the median and maximum lifespans were significantly increased in mutant males compared to WT littermates. The median lifespan was increased from 884 days to 1005 days (p = 0.006 as determined by the log rank test) and the 80% lifespan (defined here as 80% deaths) was increased from 941 days to 1073 days (p = 0.004 as determined by the Wang-Allison test). There was no difference in either median or 80% lifespan in female genotypes. WT mice of both genders became increasingly obese with age, while mutant mice maintained their lean phenotype into old age. Adiposity was found to correlate with lifespan for males only. 50% of male mice between 30 and 35 g, corresponding to about 5% body fat, for either genotype lived over 1000 days. No male mouse outside of this weight range achieved this lifespan. During their last month of life, WT mice began losing weight (a total of 8% and 15% of body weight was lost for males and females, respectively), but RIIβ?/? male mice maintained their lean body mass to end of life. This attenuation of decline was not seen in female mutant mice. Old male mutant mice were insulin sensitive throughout their life. Both genders showed modestly lower blood glucose levels in old mutants compared to WT. Male mutants were also resistant to age-induced fatty liver. Pathological assessment of tissues from end of life male mutant mice showed a decrease in tumor incidence, decreased severity of renal lesions, and a trend towards a decrease in age-related cardiac pathology. These findings help establish the highly conserved nature of PKA and suggest that disruption of PKA affects physiological mechanisms known to be associated with healthy aging.
Implosion of quadrupole gravitational waves
W. B. Bonnor,M. S. Piper
Physics , 1996,
Abstract: Einstein's vacuum equations are solved up to the second approximation for imploding quadrupole gravitational waves. The implosion generates a black hole singularity irrespective of the strength of the waves.
The gravitational wave rocket
W. B. Bonnor,M. S. Piper
Physics , 1997, DOI: 10.1088/0264-9381/14/10/015
Abstract: Einstein's equations admit solutions corresponding to photon rockets. In these a massive particle recoils because of the anisotropic emission of photons. In this paper we ask whether rocket motion can be powered only by the emission of gravitational waves. We use the double series approximation method and show that this is possible. A loss of mass and gain in momentum arise in the second approximation because of the emission of quadrupole and octupole waves.
Suppression of gravitational radiation
W. B. Bonnor,M. S. Piper
Physics , 1997, DOI: 10.1088/0264-9381/15/4/016
Abstract: We consider a burst of quadrupole gravitational radiation in the presence of a large static mass $M$ situated at its source. Some of the radiation is back-scattered off the static field of the large mass, forming a wave tail. After the burst, the tail is a pure incoming wave, carrying energy back towards the source. We calculate this energy, and, in a numerical example, compare it with the outgoing wave energy. If $M$ is sufficiently large the incoming energy can equal the outgoing energy, indicating that the primary outgoing wave is completely suppressed.
Normalized Rare Earth Elements in Water, Sediments, and Wine: Identifying Sources and Environmental Redox Conditions  [PDF]
David Z. Piper, Michael Bau
American Journal of Analytical Chemistry (AJAC) , 2013, DOI: 10.4236/ajac.2013.410A1009
Abstract: The concentrations of the rare earth elements (REE) in surface waters and sediments, when normalized on an element-by-element basis to one of several rock standards and plotted versus atomic number, yield curves that reveal their partitioning between different sediment fractions and the sources of those fractions, for example, between terrestrial-derived lithogenous debris and seawater-derived biogenous detritus and hydrogenous metal oxides. The REE of ancient sediments support their partitioning into these same fractions and further contribute to the identification of the redox geochemistry of the sea water in which the sediments accumulated. The normalized curves of the REE that have been examined in several South American wine varietals can be interpreted to reflect the lithology of the bedrock on which the vines may have been grown, suggesting limited fractionation during soil development.

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