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Relevant bibliographies by topics / Andrew Mousley

Academic literature on the topic 'Andrew Mousley'

Author: Grafiati

Published: 10 December 2022

Last updated: 29 January 2023

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Journal articles on the topic "Andrew Mousley"

1

Seyfried, Thomas N. "Mouse Brain Development. Andre M. Goffinet , Pasko Rakic." Quarterly Review of Biology 76, no. 2 (June 2001): 265–66. http://dx.doi.org/10.1086/393966.

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Miller, Malcolm. "Jerusalem, Music Centre: Andre Hajdu." Tempo 67, no. 264 (April 2013): 78. http://dx.doi.org/10.1017/s004029821300017x.

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An 80th birthday concert full of the spirit of youthful exploration reflected the innovative interactive aesthetic of Andre Hajdu, the Hungarian-Israeli composer, whose oeuvre is gradually gaining wider international exposure. Presented by the Jerusalem Music Centre on 29 March 2012, the programme featured works from the last quarter of a century for chamber duo and solo piano, including two premières, culminating in an improvisational interactive jam session by an array of students and colleagues, joined by the composer himself at the piano. To begin was Hajdu's Sonatine for Flute and Cello (1990) ‘in the French style’ performed with panache by the flautist Yossi Arnheim and cellist Amir Eldan. It is an elegantly written work radiating the spirit of Hajdu's teachers Milhaud and (less overtly) Messiaen, with whom he studied in Paris in the 1950s and 60s. Beneath the light-hearted veneer of polyphonic textures is a serious, plangent expressiveness. The first movement, libre et gai, moves from the chirpy, Poulenc-like delicacy of a cat-and-mouse imitative chase, building tension towards a final stretto. In the second movement, molto moderato, Arnheim wove a lyrical cantilena for flute over gentle cello accompaniments, giving way to rarified high cello registers shadowed by eloquent lower lines of the flute. An exuberant dance-like finale, Libre mais un peu rythmé, increased in drama before receding to a tranquil conclusion.

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Woodfield, Sarah E., Roma H. Patel, Andres F. Espinoza, Richard S. Whitlock, Jessica Epps, Andrew Badachhape, Samuel R. Larson, et al. "Abstract PO013: Patient-derived xenograft mouse models of hepatoblastoma for a personalized medicine pipeline." Clinical Cancer Research 28, no. 17_Supplement (September 1, 2022): PO013. http://dx.doi.org/10.1158/1557-3265.liverca22-po013.

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Abstract Introduction: Hepatoblastoma (HB) is the most common pediatric primary liver tumor and has the fastest rising incidence of all pediatric solid tumors. Patients with high-risk, treatment refractory, or relapse disease have a survival rate of less than 50%. The development of clinically relevant models of these aggressive tumors will facilitate studies to identify drugs that target these cells.Methods: Fresh, whole primary tumor samples were implanted into the livers of immunocompromised mice. Tumor growth was monitored with MRI and ELISA to measure serum human Alpha-fetoprotein (AFP), which is detectable in the blood of tumor-bearing animals. Tumors were validated with immunohistochemistry (IHC) for HB markers Glypican-3 (GPC3) and Beta-catenin; short tandem repeat (STR) DNA validation; next generation sequencing-based mutation profiling of 124 genes involved in pediatric solid tumors; RNA sequencing (RNA-seq), and single cell RNA-seq (scRNA-seq). Lung metastasis was also detected in models with serial sectioning and H&E staining. Cells derived from tumors were grown in vitro in adherent and spheroid conditions and used for high throughput drug screening of candidate agents. Tumors were serially passaged in animals for further in vivo drug testing of novel targeted agents.Results: Nine patient-derived xenograft (PDX) models were generated that represent low- and high-risk tumors, treatment refractory cases, and relapsed tumors. Passaging of these models showed consistent implantation rates at or above 80% with tumors detectable in 2 to 4 weeks. Eight of nine models secrete human serum AFP. All models mimic gene expression and histological patterns of their primary tumor counterparts as well as identical STR DNA profiles. The models also show gene expression consistent with an HB2/high-risk profile according to the Sumazin HB expression signature. Interestingly, two models represent unique sub-clones of a very aggressive HB relapse with different AFP secretion and transcriptomic expression. scRNA-seq of these two models indicated outgrowth of disparate disease sub-clones. The nine models also demonstrate a range of DNA mutations with three or four mutations per tumor; all variants present in the original clinical samples were conserved in the PDX models. Lung metastasis was evident in six of nine models. Two stable patient-derived cell lines (PDCLs) were developed from models, and these cell lines show expression of HB markers and secrete AFP with growth in culture. Drug screening of adherent and spheroid tumor cells support the efficacy of novel targeted agents and indicate a spectrum of sensitivity to cisplatin, a frontline standard chemotherapy agent. Importantly, the models replicate the chemotherapy responses of the corresponding patients. Additional in vitro and in vivo work showed the efficacy of a histone deacetylase inhibitor, panobinostat.Conclusions: These novel orthotopic PDX models of HB fully recapitulate the primary tumors and represent a platform for clinically relevant drug screening and testing. Citation Format: Sarah E Woodfield, Roma H Patel, Andres F Espinoza, Richard S Whitlock, Jessica Epps, Andrew Badachhape, Samuel R Larson, Rohit K Srivastava, Aayushi P Shah, Saiabhiroop R Govindu, Barry Zorman, Brandon J Mistretta, Kevin E Fisher, Ilavarasi Gandhi, Jacquelyn Reuther, Martin Urbicain, Aryana M Ibarra, Sakuni Rankothgedera, Kimberly R Holloway, Stephen F Sarabia, Andras Heczey, Ketan B Ghaghada, Kalyani R Patel, Dolores Lopez-Terrada, Angshumoy Roy, Preethi H Gunaratne, Pavel Sumazin, Sanjeev A Vasudevan. Patient-derived xenograft mouse models of hepatoblastoma for a personalized medicine pipeline [abstract]. In: Proceedings of the AACR Special Conference: Advances in the Pathogenesis and Molecular Therapies of Liver Cancer; 2022 May 5-8; Boston, MA. Philadelphia (PA): AACR; Clin Cancer Res 2022;28(17_Suppl):Abstract nr PO013.

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Kim, Rina, Ayumi Hashimoto, Nune Markosyan, Vladimir A. Tyurin, Yulia Y. Tyurina, Shuyu Fu, Mohit Sehgal, et al. "Abstract C046: Polymorphonuclear myeloid derived suppressor cells die by ferroptosis in the tumor microenvironment." Cancer Research 82, no. 22_Supplement (November 15, 2022): C046. http://dx.doi.org/10.1158/1538-7445.panca22-c046.

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Abstract Myeloid-derived suppressor cells (MDSC) in the tumor microenvironment (TME) function as an immunosuppressive shield that protects the tumor from the host’s immune system and considered a barrier to effective immunotherapy. Here, we focused on polymorphonuclear (PMN)-MDSCs, the most prevalent MDSCs in the TME, to identify mechanisms regulating their maintenance, turnover, and accumulation. Using four mouse models of cancer including autochthonous pancreatic adenocarcinoma from KPC genetically engineered mice (KrasG12D/p53R172H, PdxCre), we found that PMN-MDSCs spontaneously die by ferroptosis, a non-apoptotic form of regulated cell death triggered by the discoordination of regulatory redox mechanisms culminating in massive peroxidation of polyunsaturated phospholipids. Only PMN-MDSCs within the TME were observed to spontaneously undergo ferroptosis. In mice, ferroptosis-related gene expression in CD11b+L6ClowLy6G+ PMN-MDSC isolated from bone marrow, spleen, and tumor demonstrated tumor-specific ferroptosis across tumor models. In humans, whole transcriptomic analysis of PMN-MDSC sorted from tumors and matched blood of lung cancer patients vs blood of healthy donors revealed up-regulation of genes involved in the regulation of ferroptosis in tumor PMN-MDSC. Ferroptosis gene signatures correlated with the PMN-MDSC signatures in pancreatic cancer patients and was associated with worse overall survival. Thus, ferroptosis is an unappreciated, prominent pathway of cell death of PMN-MDSCs in cancer linked to clinical outcome in patients with pancreatic cancer. Citation Format: Rina Kim, Ayumi Hashimoto, Nune Markosyan, Vladimir A. Tyurin, Yulia Y. Tyurina, Shuyu Fu, Mohit Sehgal, Laura Garcia-Gerique, Gozde Kar, Andrew Kossenkov, Bereket A. Gebregziabher, John W. Tobias, Kristin Hicks, Hui Deng, Laxminarasimha Donthireddy, Andrew Greenberg, Brian Nam, Yulia Nefedova, Valerian E. Kagan, Robert H. Vonderheide, Dmitry Gabrilovich. Polymorphonuclear myeloid derived suppressor cells die by ferroptosis in the tumor microenvironment [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer; 2022 Sep 13-16; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2022;82(22 Suppl):Abstract nr C046.

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Bowman, John C. "Douglas Scott Falconer. 10 March 1913 – 23 February 2004." Biographical Memoirs of Fellows of the Royal Society 51 (January 2005): 119–33. http://dx.doi.org/10.1098/rsbm.2005.0008.

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Douglas Scott Falconer obtained a first–class honours degree in Zoology at St Andrews University followed by a PhD at Cambridge for research on wireworms. He then worked with R. A. (later Sir Ronald) Fisher FRS, as a prelude to joining the ARC Genetics Section of its Animal Breeding and Genetics Research Organisation at Edinburgh University. There he spent the rest of his career, later becoming Head of Unit and a personal professor in the university.His research interests fell into three main categories: the formal genetics of the mouse, quantitative genetics, and the genetics of human diseases. His work on mouse mutants and gene linkage was a major contribution to mapping the mouse genome, and his research in quantitative genetics produced theoretical and practical findings that have been of much benefit to animal breeders and to human geneticists as well as to the understanding of traits of complex inheritance.From his research and teaching he developed his acclaimed textbook Introduction to quantitative genetics , which ran to four editions in 36 years. The book is used as a foundation text worldwide.Douglas was much admired as a stimulating and innovative scientist, a considerate and polite colleague, and family gentleman.

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Choi, Sung Hee, Alicia Aguilar, Jay Myers, Byung-Gyu Kim, Saada Eid, Suzanne Tomchuck, Daniel Kingsley, and Alex Huang. "Mechanosensory channel Piezo1 is essential in pathogenic T cell-mediated intestinal inflammation." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 113.16. http://dx.doi.org/10.4049/jimmunol.208.supp.113.16.

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Abstract Inflammatory bowel disease (IBD) is a chronic inflammatory disorder in the gastrointestinal tract. CD4+ T cells are especially known to be the main drivers of IBD when they show an elevated level of activation. Elevation of intracellular Ca2+ is one of the key triggering signals for T cell activation. Piezo1 is a mechanosensitive nonselective Ca2+-permeable cation channel, which is broadly expressed in mammalian cells. However, the role of Piezo1 in the pathogenesis of T cell-mediated colitis remains unknown. We have generated T cell-specific Piezo1 knockout (Piezo1fl/flxCD4-cre) mice and observed that loss of Piezo1 in CD4+ T cell increased Th1 and Th17 cell polarization. RNA-sequence analysis of Piezo1fl/flxCD4-cre T cells identified elevated pathogenic Th17 cell pathway, IFN-γ signaling pathways and inflammatory response gene signature compared to that of wild type. These results suggest that Piezo1 controls the inflammatory response of pathogenic T cells. Next, we examined the function of Piezo1 on intestinal inflammation in vivo using acute and chronic colitis mouse model. For the acute colitis mouse model, we used a chemically induced mouse model of colitis using DSS in drinking water. Piezo1fl/flxCD4-cre mice with DSS developed severe colitis compared to Piezo1fl/fl mice with DSS. However, in chronic colitis mouse model, which is the adaptive transfer of naïve CD4+ T cells (CD4+CD45RBhigh) from Piezo1fl/fl or Piezo1fl/flxCD4cre into Rag1−/− mice, T cells from Piezo1fl/flxCD4cre mice failed to induce colon inflammation, while mice that received T cells from Piezo1fl/fl mice developed severe intestinal inflammation. Thus, our data demonstrate a critical role of Piezo1 in CD4+ T cell-mediated intestinal inflammation. Supported by R03 CA230840, P30 CA043703, St. Baldrick’s Foundation, Hyundai Hope-on-Wheels Scholar Hope Grant, Andrew McDonough B+ Foundation, Curing Kids Cancer, Center for Pediatric Immunotherapy at Rainbow

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Kim, Jin, Woo-Sung Kwon, Md Saidur Rahman, June-Sub Lee, Sung-Jae Yoon, Yoo-Jin Park, Young-Ah You, and Myung-Geol Pang. "Effect of sodium fluoride on male mouse fertility." Andrology 3, no. 3 (April 8, 2015): 544–51. http://dx.doi.org/10.1111/andr.12006.

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Dai, J., C. Zhan, W. Xu, Z. Wang, D. Nie, X. Zhao, D. Zhang, et al. "Nicotine elevates sperm motility and inducesPfn1promoter hypomethylation in mouse testis." Andrology 3, no. 5 (August 20, 2015): 967–78. http://dx.doi.org/10.1111/andr.12072.

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9

Brock, Andrew A., Katherine Powell, Thomas D. Schmittgen, and Lorenzo F. Sempere. "Abstract 5821: Enhanced tumorigenesis in a novel miR-216a knockout/KPC mouse model of pancreatic cancer." Cancer Research 82, no. 12_Supplement (June 15, 2022): 5821. http://dx.doi.org/10.1158/1538-7445.am2022-5821.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) originates from both ductal and acinar cells of the pancreas. The highly abundant and acinar cell-enriched miR-216a is reduced during in vitro acinar ductal metaplasia (ADM), throughout PanIN progression, during the development of pancreatitis in mice and humans, and during development of mouse and human PDAC. To investigate the contribution of miR-216a in the development of PDAC, we generated a miR-216a germline knockout mouse (216aKO) via CRISPR genetic editing of a minimal and precise deletion of the miR-216a precursor sequence without affecting the host gene. We crossed this 216aKO mouse to the LSL-KrasG12D; LSL-Trp53Flox/+; Pdx1Cre/+ (KPC) mice to produce a transgenic mouse with an activating Kras mutation, p53 deletion, and knockout of miR-216a (referred to here as miR216aKPC). miR216aKPC displayed an increase in tumor progression compared to KPC and had reduced survival - median 15 weeks miR216aKPC vs. 25 weeks for KPC. miR216aKPC produced lung metastasis by 12 weeks of age which were not present in the lungs of similarly aged KPC mice. Transfection of miR-216a mimetic oligo into cell lines derived from KPC or 216aKPC mice did not reduce viability or alter cellular morphology, suggesting that a potential tumor suppressive role of miR-216a functions during the early stages of PDAC development. A three dimensional ADM assay using acinar cells derived from both mouse and human pancreata will be applied to investigate the contributions of miR-216a on the development of ADM and cell polarity. To discover miR-216a target genes that are responsible for the increased tumorigenesis, cell lines derived from miR216aKPC will be transfected with miR-216a mimetic or scrambled control oligo followed by RNA sequencing. Our results thus far suggest a tumor suppressive role for miR-216a in the early development of PDAC and future studies will investigate molecular and cellular mechanisms driving acinar cell-induced PDAC. Citation Format: Andrew A. Brock, Katherine Powell, Thomas D. Schmittgen, Lorenzo F. Sempere. Enhanced tumorigenesis in a novel miR-216a knockout/KPC mouse model of pancreatic cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5821.

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Raza, Qanber, Michael Cohen, Smriti Kala, Liang Lim, Geneve Awong, Andrew Quong, and Christina Loh. "Abstract 2035: Imaging mass cytometry identifies structural and cellular composition of the mouse tissue microenvironment." Cancer Research 82, no. 12_Supplement (June 15, 2022): 2035. http://dx.doi.org/10.1158/1538-7445.am2022-2035.

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Abstract Imaging Mass Cytometry™ (IMC™) is a vital tool to deeply characterize the complexity and diversity of any tissue without disrupting spatial context. The Hyperion™ Imaging System utilizes IMC, based on CyTOF® technology, to simultaneously assess up to 40 individual structural and functional markers in tissues, providing unprecedented insight into the organization and function of tissue microenvironment. We have previously demonstrated the application of IMC in combination with Maxpar® panel kits to highlight cellular composition of human tissues. Here, we showcase the recently released Maxpar OnDemand Antibodies for IMC application on mouse tissue. We introduced 11 additional biomarkers to our existing mouse antibody catalog, providing the basis for the use of high-multiplex imaging in preclinical investigations. To demonstrate the IMC workflow on mouse tissue, we analyzed a normal mouse tissue microarray using IMC spatial proteomic analysis. Tissues were stained with a 20-marker panel designed to highlight tissue architecture and major immune lineage markers combined with our IMC Cell Segmentation Kit*. The IMC Cell Segmentation Kit facilitates identification of cellular borders using plasma membrane markers that lead to improved nucleus and plasma membrane demarcation. We generated a detailed spatial map of the heterogeneous tissue architecture and successfully identified immune, epithelial, and stromal cell populations in various mouse tissues. Additionally, we classified the activation state of immune cell populations, adhesion state of epithelial cells, and molecular composition of the extracellular matrix.Overall, this work demonstrates the capability of IMC to identify subcellular localization of cellular and structural markers in the mouse tissue microenvironment. Information gained from IMC studies will enable in-depth high-throughput phenotypic characterization of the tissue microenvironment in various mouse models of development and disease, and thus accelerate preclinical discoveries. *The IMC Cell Segmentation Kit is part of the Innovative Solutions menu of custom-made reagents and workflows developed and tested by Fluidigm scientists to give faster access to new cutting-edge solutions for high-multiplex single-cell analysis. Innovative Solutions are not part of the Maxpar catalog. For Research Use Only. Not for use in diagnostic procedures. Citation Format: Qanber Raza, Michael Cohen, Smriti Kala, Liang Lim, Geneve Awong, Andrew Quong, Christina Loh. Imaging mass cytometry identifies structural and cellular composition of the mouse tissue microenvironment [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2035.

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Dissertations / Theses on the topic "Andrew Mousley"

1

Mousser, Jaouad [Verfasser]. "A Large Coverage Verb Lexicon For Arabic / Jaouad Mousser." Konstanz : Bibliothek der Universität Konstanz, 2015. http://d-nb.info/1099956943/34.

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Widner-Andrä, Regina [Verfasser], and Rainer [Akademischer Betreuer] Landgraf. "Assignment of functional impact on genetic data in two mouse models of affective disorders / Regina Andrea Widner-Andrä. Betreuer: Rainer Landgraf." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2012. http://d-nb.info/1023435535/34.

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Jin, Wen [Verfasser], Wolfgang [Akademischer Betreuer] Baumgärtner, Andrea [Akademischer Betreuer] Tipold, and Kirsten [Akademischer Betreuer] Haastert-Talini. "Intraspinal Infection with Theiler’s Murine Encephalomyelitis Virus in Resistant and Susceptible Mouse Strains / Wen Jin ; Wolfgang Baumgärtner, Andrea Tipold, Kirsten Haastert-Talini." Hannover : Stiftung Tierärztliche Hochschule Hannover, 2020. http://d-nb.info/122488292X/34.

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Hipp, Silvia Andrea [Verfasser]. "Influence of different types of amyloid β pathologies on tau pathology in Alzheimer´s disease in different APP-TAU double transgenic mouse models / Silvia Andrea Hipp." Ulm : Universität Ulm, 2018. http://d-nb.info/1166757242/34.

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Forero, Echeverry Andrea [Verfasser], Klaus-Peter [Gutachter] Lesch, Markus [Gutachter] Sauer, and Robert [Gutachter] Blum. "Impact of Cadherin-13 deficiency on the brain serotonin system using mouse models and human iPSC-derived neurons / Andrea Forero Echeverry ; Gutachter: Klaus-Peter Lesch, Markus Sauer, Robert Blum." Würzburg : Universität Würzburg, 2020. http://d-nb.info/1221963287/34.

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Zweck, Jonathan Mark. "This old man." Thesis, 2017. http://hdl.handle.net/2440/112812.

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This Old Man is comprised of a childhood section from a larger novel that interweaves the experiences of a group of childhood friends who, as adults, are compelled to return to their home town to face an evil they were haunted by as children. Due to word count constraints, the chapters submitted for the Thesis are from the ‘childhood section’ of the novel only. The novel in its entirety explores how adult selves are shaped by their past experiences. This first thematic drive is explored alongside another, which focusses on ideas of agency and humanity in the face of these deterministic forces. The larger work responds to Stephen King’s IT. It employs the tropes of the Horror genre to tell a story about manhood, boyhood, and what happens in between; a story about the summer when, as kids, the characters were hunted by The Farmer and his Doberman, and the summer nearly twenty years later when they return to finish the battle as adults: adults with inner demons that may prove to be stronger than the Farmer himself; adults who are facing the traumas of their past and attempting to find the capacity to forge and maintain relationships; adults who must finally grow up and accept responsibility for their actions and the fate of their lives. ‘An Act of Reading and Writing’ Why am I drawn to heroic genre fiction? Why did I choose it as a mode to explore agency? And why did Horror end up being the mode in which to do it? What is it about the reinvention of these familiar structures that on the one hand fills a deep need for stability, but on the other challenges the way I think about the world? Why do reading and writing act as a meditative process? What is it about fiction that evades essentialism, and how do prescriptive structures like the Hero’s Journey act as a meditative space that open themselves up to interpret the world around us? This exegesis explores these questions through a framework of discussions with texts that informed my work. Using a humanist framework centred on the agency of the individual to affect change, as argued for by Edward Said, I explore how literature acts as a kind of humanist theology in the post-modern world, as envisaged by Andy Mousley. I then explore how heroic structures in genre fiction might be a meditation on agency.
Thesis (Ph.D.) -- University of Adelaide, School of Humanities, 2017.

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Schwaiger, Andrea [Verfasser]. "Biomedizinische Anwendungen der NMR-MOUSE / vorgelegt von Andrea Schwaiger." 2002. http://d-nb.info/967064333/34.

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Croxford, Andrew Lewis [Verfasser]. "Novel mouse models for use in IL-17A and Th17 research / Andrew Lewis Croxford." 2009. http://d-nb.info/1005380252/34.

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Andre, Philipp [Verfasser]. "Delimitation of the organizer from the posterior notochord : descriptive and functional studies in mouse and African clawed frog / vorgelegt von Philipp Andre." 2009. http://d-nb.info/999426990/34.

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Books on the topic "Andrew Mousley"

1

Andrew Warhol: Micky Mouse (Print Book). Te Neues Pub Group, 1995.

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2

Crothers, Keith. Adventures of Andrew the Church House Mouse: Andrew's First Adventure. Independently Published, 2018.

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Hipp, Andrew, and Dwight Kuhn. The Life Cycle of a Mouse (Hipp, Andrew. Life Cycles Library.). Rosen Publishing Group, 2002.

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