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1
Wang, Mengdong. "Studies on IgA Induction in Intestine and Mammary Glands of Mammals." Kyoto University, 2015. http://hdl.handle.net/2433/199345.
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Kyoto University (京都大学)0048
新制・課程博士
博士(農学)
甲第19021号
農博第2099号
新制||農||1030(附属図書館)
学位論文||H27||N4903(農学部図書室)
31972
京都大学大学院農学研究科応用生物科学専攻
(主査)教授 久米 新一, 教授 祝前 博明, 教授 廣岡 博之
学位規則第4条第1項該当
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Miao, Yu Rebecca. "The role of c-Myb in mammary gland development and tumourigenesis." Connect to thesis, 2009. http://repository.unimelb.edu.au/10187/7069.
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c-Myb/MYB is an established and key player in hematopoietic malignancies but more recently a strong case for c-Myb as an oncogene in breast cancer has emerged. c-Myb and its transcriptional target genes have direct bearing on tumour initiation and progression and thus this has opened new opportunities to the development of therapeutic approaches in a range of cancer types with the aim of treating cancer at its various stages. In this study, the requirement of c-Myb during mammary gland tumourigenesis is being examined. In addition a direct therapeutic approach to targeting c-Myb-driven gene grp78/GRP78 in the context of primary and metastatic breast cancer was assessed.The first aim of this study is to examine the expression of c-Myb during normal mammary gland development. The expression of c-Myb is extensively characterised in a temporal and spatial fashion. Nuclear staining of c-Myb by immunohistochemisty was found to be most elaborately expressed in the ductal epithelium during early mammary gland development. Mouse mammary gland lacking c-myb showed disorganised ductal structure in virgin mice, but did not affect subsequent pregnancy and lactation.
To extend the view that c-Myb is involved in mammary tumourigenesis c-myb-transduced immortalised mammary epithelial cells and two mammary tumour prone transgenic mouse models were examined. NMuMG cells transduced with c-myb showed enhanced proliferation and reduced Annexin V staining consistent with the protection from apoptosis. This reduced apoptosis is consistent with, and perhaps contingent upon, the elevated expression observed for bcl-2 and grp78. The data assembled by expression studies raised the possibility that c-Myb is essential for the establishment of mammary gland tumor in both MMTV-Neu and MMTV-PyMT spontaneous mammary gland tumor models. Loss of c-Myb expression in these models significantly delayed and in most instances completely abolished the onset of mammary gland tumours in both models. Preliminary evidence also indicated that Stat3 phosphorylation may underpin the elevated c-Myb expression in mouse mammary tumour cells.
The focus of my thesis then shifted to examining ways to exploit elevated c-Myb target gene GRP78 expression on the cell surface of mammary tumour cells. To do this I employed a GRP78 binding pro-apoptotic chimera peptide that specifically binds to GRP78 where I examined its efficacy against primary and metastatic breast cancer models. My results demonstrated the anti-tumour activity of the GRP78-chimera peptide both in vitro and in vivo. More importantly, the peptide is also effective at prolonging disease-free survival in mice with established metastatic disease.
Evidence obtained within these studies suggests that c-Myb plays an important role in mammary gland development and tumourgenesis. Although it may be difficult to directly target c-Myb in malignant disease, alternative anti-tumoural therapy may be developed against c-Myb-regulated target genes that are also implicated in mammary tumours. Collectively my thesis studies have advanced our understanding of c-Myb in mammary cancer initiation, progression and as a direct or indirect therapeutic target.
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Aupperlee, Mark Douglas. "The regulation and function of progesterone receptor isoforms A and B in the normal mouse mammary gland." Diss., Connect to online resource - MSU authorized users, 2008.
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Thesis (Ph. D.)--Michigan State University. Cell and Molecular Biology Program, 2008.Title from PDF t.p. (viewed on March 30, 2009) Includes bibliographical references (p. 174-178). Also issued in print.
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Raghuraman, Nandini. "Prepubertal bisphenol A exposure in the rat mammary gland mechanism of action for carcinogenesis /." Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2009r/raghuraman.pdf.
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Nemir, Mohamed. "Inhibition of osteopontin expression in mammary epithelial cells alters mammary gland morphogenesis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0020/NQ44529.pdf.
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Smith, Diane H. "Insulin receptors in the mammary gland /." The Ohio State University, 1986. http://rave.ohiolink.edu/etdc/view?acc_num=osu148726802174716.
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Frend, Hayley Theresa. "Mammary gland hierarchy and its controlling mechanisms." Thesis, University of Cambridge, 2014. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708178.
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Hughes, Katherine. "Inflammation and remodelling in mammary gland involution." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607688.
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Wang, Juexuan. "Characterization of BCL11 functions in the mouse mammary gland identifies two types of mammary stem cells." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610044.
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Enger, Benjamin David. "Intramammary infection in rapidly growing, non-lactating mammary glands." Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/96306.
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Intramammary infections (IMI) are common in non-lactating heifer and dry cow mammary glands and occur during periods of appreciable mammary growth and development. The presence of these infections is expected to negatively impact mammary growth and development but has yet to be investigated. The works reported here investigated how IMI affects mammary tissue structure, cellularity, and the expression of integral mammogenic hormone receptors implicated in mammary growth. Non-pregnant non-lactating cows (n = 19) were administered estradiol and progesterone to stimulate mammary growth and 2 quarters of each cow were subsequently infused with either saline (n = 19) or Staphylococcus aureus (n = 19). Intramammary infusion of Staphylococcus aureus increased the number of immune cells present in gland secretions and also increased the proportion of neutrophils comprising these secretion somatic cells. Mammary tissues from quarters infused with Staphylococcus aureus contained more immune cells, less mammary epithelial tissue area, and greater tissue areas of intralobular stromal tissue than saline quarters. Staphylococcus aureus quarters also contained more apoptotic mammary epithelial cells and a lower proportion of apoptotic cells in the intralobular stroma compartment than saline infused quarters; this signified that Staphylococcus aureus quarters had less epithelial growth and experienced an expansion and/or lack of regression of stromal tissues. The number of cells expressing estrogen receptor α (ESR1) and progesterone receptor (PGR), as well as staining characteristics of ESR1 and PGR positive nuclei was also examined in these tissues. No appreciable differences were observed in any of the examined ESR1 and PGR measures between Staphylococcus aureus and saline mammary glands, but myoepithelial cells from Staphylococcus aureus glands had a greater nuclear staining area than saline quarters, indicating that these cells were affected by IMI. The results of these investigations indicate that IMI, in mammary glands that are concurrently stimulated to grow and develop, limits the growth of mammary epithelium and impairs regression of the stromal tissue, both of which are necessary for successful lactational performance.PHD
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Kreuzaler, Peter Anton. "Cell death modalities in mammary gland involution." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609378.
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Smith, James Joseph. "An investigation into hormonal regulation of ovine mammary gland growth during pregnancy." Thesis, Virginia Tech, 1985. http://hdl.handle.net/10919/41561.
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Prepartum, multiparous ewes were randomly assigned to experimental groups and sacrificed at 50(n=5), SO(n=4),115(n=5), and 140(n=4) days of gestation. Serum harvested the week prior to slaughter was assayed for progesterone (PG), prolactin (PRL) and growth hormone (GH) concentrations. Mammary tissue obtained at slaughter was assayed for receptor concentrations of progesterone (PGr), prolactin (PRLr) and insulin (Ir). Quantitative biochemical, histological and autoradiographical analyses were used to measure mammary gland growth and indicated no significant glandular growth occurs prior to 8O days of gestation. However, a major phase of parenchymal growth occurred between 8O and 115 days which coincided with significant increases in PG, PGr and PRLr concentrations. Parenchymal growth continued further into late pregnancy. GH and Ir concentrations did not change significantly during pregnancy and were not strongly correlated to growth measurements. These results suggest that mammary gland growth is receptor-mediated and direct or indirect regulation of PGr and PRLr is primarily responsible for the observed growth phenomenon.Master of Science
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Patel, Amita. "Transcriptional regulation of cathepsin L during mouse mammary gland involution a test of STAT3 involvement /." Click here for download, 2006. http://wwwlib.umi.com/cr/villanova/fullcit?p1432835.
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Stairiker, Patricia A. "The role of L in involution and the termination of lactation in the mouse mammary gland." Click here for download, 2007. http://proquest.umi.com/pqdweb?did=1075710531&sid=3&Fmt=2&clientId=3260&RQT=309&VName=PQD.
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Li, Wenjing. "The role of PML and executioner caspases in mammary gland development." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609289.
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Ward, David 1968. "A quantitative study on the uptake of nutrients in the mammary gland of the cow." Thesis, The University of Sydney, 1997. https://hdl.handle.net/2123/27639.
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Hedengran, Faulds Malin. "Estrogen receptor signalling in mammary epithelial cells /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-936-6/.
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Stairiker, Patricia A. "The role of cathepsin L in involution and the termination of lactation in the mouse mammary gland." Click here for download, 2006. http://wwwlib.umi.com/cr/villanova/fullcit?p1432836.
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Gaddis, Christine A. "Development and use of an in vivo mouse model system to assess the morphological effects of exposure to endocrine disrupting compounds in uterine and mammary tissue." Click here for download, 2008. http://proquest.umi.com/pqdweb?did=1633784231&sid=1&Fmt=2&clientId=3260&RQT=309&VName=PQD.
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Higginbotham, Anderson Lisa Ann. "Cell fate determination in the mouse mammary gland." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609183.
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Demicco, Elizabeth G. "Non-classical nuclear factor-kappa B complexes in mammary gland development and tumorigenesis." Thesis, Boston University, 2005. https://hdl.handle.net/2144/37131.
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Thesis (Ph.D.)--Boston UniversityPLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
Post-natal mammary gland development is a complex process in which epithelial proliferation and branching of lactiferous ducts is followed by extensive formation of lobuloalveolar units that produce milk. Classical nuclear factor-kappa B (NF-κB) p65/p50 transcription factors are dynamically induced in the mammary gland during pregnancy, and inhibitor of NF-κB-alpha (IκB-α) deficiency leads to hyperplasia of the mammary epithelium. To further elucidate the role of NF-κB factors in mammary development, we examined NF-κB subunit expression in the mammary glands of transgenic mice expressing the IκB-α S32/36A super-repressor (SR) protein under control of the mouse mammary tumor virus (MMTV)-long terminal repeat promoter, in which mammary gland development is transiently delayed, but not completely blocked. Developmental recovery correlated with induction of RelB/p52 NF-κB complexes, which failed to interact with an IκB-α fusion protein and potently induced cyclin D1 and c-myc promoter activities. Activation of IκB-α kinase alpha (IKKα) and NF-κB inducing kinase (NIK) was detected by day 5.5, and were hypothesized to be responsible for the induction of ReIB/p52. In support of this hypothesis, we found that constitutively active IKKα induced p52, RelB, and cyclin D1 in untransformed mammary epithelial cells. Moreover, mammary tumors induced by high-dose 7,12-dimethylbenz(a)anthracene (DMBA) treatment in wild type FVB/N mice, displayed increased RelB/p52 binding activity. These results implicate activation of RelB/p52 complexes by the alternative NF-κB signaling pathway in branching of lateral ducts and alveolar development during mammary gland development, and in mammary carcinogenesis.
2031-01-01
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Giraddi, Rajashekharagouda. "Cell cycle kinetics of mammary stem and progenitor cells." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607789.
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Webster, Marc A. "Mechanisms of polyomavirus transformation of the mouse mammary gland /." *McMaster only, 1996.
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Woodward, Terry L. "Effects of ovarian steroids on bovine mammary epithelial cells : in vitro and in viro evidence of indirect stimulation of proliferation /." Thesis, Virginia Tech, 1991. http://hdl.handle.net/10919/41629.
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Three studies were conducted to determine the effects of ovarian steroids on bovine mammary epithelial cell proliferation. In a first study, estrogen (E), progesterone (P), or E+P were administered to prepubertal beef heifers and biopsied mammary parenchyma taken before and following treatment were compared for growth by evaluation of histoautoradiographic incorporation of thymidine. Estrogen increased epithelial cell growth by 24 h, and fibroblasts to a lesser magnitude by 48-96 h. Estrogen and P was less effective and P was ineffective in increasing proliferation in all cell types studied. Proliferation of adipocytes was not altered.
A second study characterized hormone responsive proliferation of Mac-T cells, a recent clonal bovine mammary epithelial cell strain. Mac-T cells responded to all hormones tested as would be expected in vivo. Additionally, passage, harvesting, quantification, freezing, and co-culture techniques were modified to facilitate uncomplicated, timely, inexpensive, effective testing of growth responsiveness to hormones or growth factors.
In a third study E and P alone, together, with or without serum were unable to increase Mac-T cell proliferation. Serum from prepubertal Holstein heifers after E treatment did not increase growth of Mac-T cells over serum before treatment. Conditioned media from Mac-T or Fib-T (mammary bovine fibroblast cell line) with or without steroids were tested for ability to increase Mac-T cell proliferation. Growth of Mac-T cells was greatest in Fib-T + E conditioned media followed by Fib-T, then Mac-T and lastly fresh media. Steroid exposure did not enhance the ability of Mac-T cell conditioned media to increase Mac-T cell proliferation.
In conclusion, E appears to be the primary ovarian steroid involved in initiating bovine mammogenesis. However, estrogen’s action is not direct and may be caused by paracrine release of growth factors.Master of Science
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Staniszewska, Anna Dominika. "Roles of Stat3 in mammary gland development, involution and breast cancer." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610277.
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Roarty, Kevin Patrick. "The role of TGF-ß and Wnt5a in mammary gland development and tumorigenesis." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2008p/roarty.pdf.
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Pascual, Domingo Rosa. "CPEB2 in mammary gland homeostasis and breast cancer." Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/586313.
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The mammary gland develops postnatally and is remodeled, during each estrous cycle and pregnancy, through very dynamic expansions and involutions of its polarized epithelial tree. Moreover, the mammary gland is hierarchically organized, where the two main epithelial populations may arise from a common bipotent mammary stem cell (MaSC). The principal epithelial cell types in the mammary gland are luminal cells and myoepithelial cells (also named basal cells), which are found surrounding luminal cells and in contact with the extracellular matrix. Further, the luminal compartment has two main lineages: the alveolar lineage in charge of producing milk during lactation, and the ductal lineage that include the cells that express receptors of the ovarian hormones like estrogen and progesterone. Interestingly, each of these luminal lineages is sustained by their own progenitors. Thus, the mammary gland requires a tightly regulated balance between proliferation and differentiation, which is disrupted in breast tumors. Distinct transcriptional circuits orchestrating such finely tuned processes have been described; however, how translational control contributes to mammary gland homeostasis and tumorigenesis remains largely unexplored.
The CPEB-family (Cytoplasmic Polyadenylation Element Binding Proteins) of RNA- binding proteins (RBPs) is composed of four members in vertebrates (CPEB1-4); differentially, in Drosophila Melanogaster, there are two CPEB orthologs (Orb and Orb2). Within the CPEB-family, there are two subfamilies based on sequence identity of the RNA recognition motifs: CPEB1 and CPEB2-4. CPEB proteins share the same RNA- binding C-terminal domain (CTD), while they differ on their unstructured regulatory N- terminal domain (NTD). This fact has two significant implications: CPEBs can bind overlapping target mRNAs by recognizing CPEs in the 3’UTR; however, they are regulated by different post-transcriptional modifications at the NTD that will be triggered by distinct signaling pathways. Therefore, CPEB proteins could compete against one another for the binding, act sequentially on the same target mRNA or even
compensate the loss of one member of the CPEB-family. CPEBs regulated cytoplasmic polyadenylation by recognizing a motif called Cytoplasmic Polyadenylation Element (CPE) present in the 3’UTR of certain mRNAs. Remarkably, CPEBs can potentially regulate up to 25% of the genome and they can control translation of CPEB-bound mRNAs in time and subcellular space. Furthermore, CPEB proteins play pivotal roles in cell proliferation and lineage-specification. Therefore, the study of the CPEBs in a hierarchically organized tissue undergoing a lot of proliferation and remodeling like the mammary epithelia may shed light on novel functions of this family of RBPs. The main goal of this study is to analyze in vivo the contribution of the four members of the CPEB-family of RNA-binding proteins in mammary epithelial morphodynamics.
Here we present a systematic study of the four members of the CPEB family (CPEB1-4) in the context of the adult mammary gland in vivo, using Knock-out (KO) models for all four CPEBs. By mammary wholemounts and flow cytometry analysis, we discovered that the lack of CPEB2 resulted in defects in mammary gland branching and lineage specification. Interestingly, CPEB2 depletion also had consequences for breast tumorigenesis. Moreover, were able to identify the target mRNAs bound by CPEB2 in mammary epithelial cells and to establish a molecular mechanism by which CPEB2 regulates mammary gland homeostasis and breast cancer.
Altogether, this work unravels a novel translational mechanism regulating cell fate in the mammary gland and breast tumor development.La glándula mamaria es el único órgano que se desarrolla principalmente después del nacimiento y, además, se remodela durante cada ciclo menstrual y embarazo a través de expansiones e involuciones muy dinámicas del epitelio polarizado que la constituye. Por lo tanto, la glándula mamaria requiere un equilibrio finamente regulado entre proliferación y diferenciación. Este equilibro se encuentra perturbado en casos de cáncer de mama. De qué manera el control tradicional contribuye a la homeostasis y tumorigenesis de la glándula mamaria es un terreno por explorar. La familia de proteínas CPEBs (Cytoplasmic Polyadenylation Element Binding) incluye cuatro proteínas de unión al RNA mensajero que regulan, de manera temporal y espacial, la traducción y la localización sub-celular de los mRNAs que unen. Las CPEBs podrían regular hasta el 25% del genoma. Aquí presentamos un estudio sistemático de los cuatro miembro de la familia de las CPEBs (CPEB1-4) en el contexto de la glándula mamaria adulta, utilizando modelos knock-out (KO) en ratón. Durante esta investigación hemos descubierto que la falta de CPEB2 resulta en defectos en las ramificaciones de la glándula mamaria, y también en diferenciación. De manera muy relevante, la depleción de CPEB2 tiene consecuencias en cáncer de mama. En conclusión, es trabajo descifra un nuevo mecanismo a nivel de traducción responsable de la regulación de la homeostasis y el desarrollo de tumores en la glándula mamaria.
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Smith, Scott Alan. "Effects of dietary fatty acids on cholesterol content, and fatty acid distributions in total and phospholipid fractions of mammary glands and adenocarcinomas from strain A/St mice." Virtual Press, 1986. http://liblink.bsu.edu/uhtbin/catkey/471160.
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This study was designed to determine the distribution of fatty acids and cholesterol in total tumor and mammary tissues. Fatty acid profiles of phospholipid fractions from tumors and mammary glands were also determined. Fatty acids and cholesterols were analyzed by gas liquid chromatography. Methodology was developed for phospholipid separation by high performance liquid chromatography.Tumors derived from mammary glands in Strain A/ST mice were found to contain two to three times the amount of cholesterol compared to normal mammary glands. Mammary glands from safflower fed mice contained significantly higher percentages of linoleic acid. Linoleic acid content in stearicacid (SA-1) fed mice was sharply reduced. linoleic acid in mammary glands of animals fed a high fat Stearic acid (SA-4) , corn oil and stock diet fed animals displayed similar fatty acid profiles. Fatty acid analysis of tumors excised from mice fed the experimental diets showed similar patterns in comparison to normal mammary glands. The similar distributions were in the 18 carbon fatty acids. Distributions of phospholipid fatty acids in tumors and mammary glands were similar. Mammary gland phospholipids displayed increased percentages of short chain (14 carbons and under) fatty acids. Results of these studies demonstrate an increased availability of diet rich in polyunsaturated fatty acids.
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Raber, James Marvin. "Molecular and cellular investigations into the strain related differences in susceptibility to mammary gland carcinogenesis /." The Ohio State University, 1986. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487265143148177.
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Daniel, Thomas Earl. "Histological evaluation of ovine mammary tissue xenografted into cyclosporine treated mice." Thesis, Virginia Tech, 1988. http://hdl.handle.net/10919/43398.
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Kutanzi, Kristy, and University of Lethbridge Faculty of Arts and Science. "The role of epigenetics in the rat mammary gland." Thesis, Lethbridge, Alta. : University of Lethbridge, Dept. of Biological Sciences, c2010, 2010. http://hdl.handle.net/10133/2492.
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Epigenetics plays an important role in carcinogenesis with heritable changes in DNA methylation and histone modifications intricately linked to the initiation, promotion, and progression of cancer. Evidence shows that a number of chemical and physical agents can induce epigenetic changes during carcinogenesis. Two such agents, estrogen and ionizing radiation, are generally recognized as being carcinogenic. Yet the epigenetic repercussions of these carcinogens remain relatively unknown. More importantly, the combined effect of these carcinogens has never been addressed in vivo from an epigenetic standpoint. Therefore, we focused on the effect of estrogen and ionizing radiation applied separately or in conjunction. We have found that the exposure to estrogen, either alone or in combination with radiation, induced pronounced morphological alterations, which was paralleled by modifications to the epigenomic landscape in the mammary gland. The results obtained from these rodent models can potentially be extrapolated to humans.xiv, 190 leaves : ill. (chiefly col.) ; 29 cm
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Olsen, Hanne. "STAT5A expression and regulation in mammary epithelial cells /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-749-5/.
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Oakes, Samantha Richelle St Vincent's Clinical School UNSW. "Investigation of the role of prolactin in mammary gland development and carcinogenesis." Awarded by:University of New South Wales. St. Vincent's Clinical School, 2006. http://handle.unsw.edu.au/1959.4/28846.
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The pituitary hormone prolactin (Prl) is essential for alveolar morphogenesis and plays a role in breast carcinogenesis, however the mechanism that underlies these actions remains to be defined. Alterations in serum Prl provide the primary endocrine signal regulating developmental events in the mammary gland in sexually mature mammals. Prl production and post-translational phosphorylation by the pituitary is regulated by the neuropeptide Galanin (Gal) in response to hypothalamic signals integrating neuronal and endocrine inputs. Prl exerts its effects on the mammary epithelium in two ways, indirectly by modulation of the systemic hormonal environment, for example the release of progesterone from the corpus luteum, and directly by binding to Prl receptors (Prlr) within the mammary epithelium. Prl binding to Prlr initiates signalling predominantly via activation of the Jak2/Stat5 pathway, leading to altered patterns of gene transcription. One of these target genes is the ets transcription factor Elf5, which is required by the epithelium for alveolar morphogenesis. This thesis aims to further our understanding of the mechanisms by which prolactin exerts its influence on the mammary gland during alveolar morphogenesis and carcinogenesis. Transcript profiling revealed a lactation signature of 35 genes in Prlr+/- mice, Gal-/- mice and mice treated with a Prl mutant (S179D) that mimics phosphorylated Prl. We discovered that the majority of changes in gene expression were produced by prolactin rather than by Gal. The action of Gal was predominantly via modulation of Prl phosphorylation and release, as its effects were very similar to that of S179D. Knockout of Elf5 phenocopied knockout of Prlr, resulting in failure of alveolar morphogenesis and reduced expression of milk and lipid synthesis genes. Forced Elf5 expression at puberty resulted in aberrant differentiation of the terminal end buds and milk protein synthesis during ductal morphogenesis. Re-expression of Elf5 in Prlr-/- mammary epithelial cells completely rescued alveolar morphogenesis. These observations indicate that Elf5 is a master regulator of alveolar morphogenesis downstream of the Prlr. Loss of mammary epithelial Prlr resulted in reduced proliferation of low-grade neoplastic lesions resulting in increased tumour latency in the C3(1)/SV40T model of mammary carcinogenesis. There was no change in the growth rate, proliferation nor the morphology of tumours in Prlr-/-/C3(1)/SV40T transplants, thus Prl acts early in carcinogenesis to drive the proliferation of pre-invasive lesions resulting in faster progression to cancer.
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Swanson, Kara M., and n/a. "The bovine mammary gland immune response to Streptococcus uberis and its bacteriocins." University of Otago. Department of Microbiology & Immunology, 2008. http://adt.otago.ac.nz./public/adt-NZDU20080407.112302.
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Bovine mastitis is one of the most costly dairy-based diseases worldwide. Streptococcus uberis is a prevalent causative organism of mastitis and resides naturally in the environment of the dairy cow making prevention of the disease difficult. New strategies need to be developed to control this pathogen. However, a fundamental understanding of the complex relationships that exist between the cow, the pathogen and the environment are required in order to advance the development of prevention strategies. Microarray technology was used to evaluate the complex transcriptional changes which occur in the bovine mammary gland following the onset of clinical S. uberis mastitis. A 22,000 bovine cDNA microarray indicated that S. uberis mastitis led to the up-regulation of 1,283 genes and the down-regulation of 1,237 genes by greater than 1.5 fold. Gene ontology analysis demonstrated that S. uberis mastitis was typically associated with the up-regulation of genes that are involved in the immune response and homeostasis and a down-regulation of genes involved in lipid metabolism. Quantitative real-time analyses for a selection of genes associated with the immune response validated the microarray data. Mammary epithelial cell cultures did not show an increase in the expression of any of these immune factors in response to the same S. uberis strain used to induce clinical mastitis. This indicates that the expression of immune-related genes by mammary epithelial cells may be initiated by host factors and not S. uberis.
The application of bacteriocins, proteinaceous antimicrobials produced by bacteria which typically inhibit the same or closely-related species to that of the producer organism, has been suggested as one possible approach in the control of mastitis. S. uberis have been previously found to commonly produce bacteriocin-like inhibitory substances (BLIS). The BLIS activities of a set of fifteen S. uberis and S. bovis strains were assessed. The results confirmed the prolific and varied nature of BLIS production by S. uberis and S. bovis and also indicated that these strains may commonly produce more than one inhibitory agent. This survey of BLIS production led to the detection and characterisation of a novel circular bacteriocin, uberolysin, produced by S. uberis strains 233 and 42. The structural gene of uberolysin was subsequently identified in nine (64%) of the fifteen test strains.
Multiplex PCR analysis showed that 93% of 158 New Zealand S. uberis isolates contained the structural genes of at least one of the four known S. uberis bacteriocins (uberolysin, nisin U, ubericin A and ubericin 63). However, no apparent direct association was identified between any one of these bacteriocin-related loci and apparent ability to cause mastitis on New Zealand dairy farms. The uberolysin structural gene was detected in 91% of the isolates and this widespread distribution prompted the advancement and evaluation of a potential role for uberolysin in immunomodulation within the bovine mammary gland. Two different preparations of uberolysin were found to have different stimulatory effects on monocytes, neutrophils and epithelial cells. The less highly purified preparation appeared to diminish the production of TNF-α by monocytes in the presence of a bacterial stimulus and to decrease neutrophil phagocytosis. By contrast, the relatively more highly purified preparation of uberolysin itself induced a significant immune response by monocytes. Consistent with this, the purer preparation of uberolysin induced an increase in C3, IL-1β, IL-6, IL-8, the β-defensin LAP, the acute-phase protein MSAA, the calcium-binding protein S100A12 and TLR2 by quantitative real-time analysis.
Although currently only two S. uberis bacteriocins (uberolysin and nisin U) have been fully characterised, the present study has shown that this species may be an important source of novel antimicrobials. Furthermore, bacteriocin production by S. uberis may have an immunomodulation role within the mammary gland. A better understanding of the complex immune response initiated at the onset of clinical S. uberis mastitis and of the role that bacteriocins have in S. uberis pathogenesis may lead to development of improved strategies to combat this disease.
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Hutchinson, John N. G. Muller William J. "The role of the Akt-1 serine/threonine kinase in mammary gland development and tumorigenesis /." *McMaster only, 2003.
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LIMA, MATEUS H. de. "Caracterização de uma câmara de ionização ar-livre em feixes diretos de raios X utilizados em mamografia." reponame:Repositório Institucional do IPEN, 2014. http://repositorio.ipen.br:8080/xmlui/handle/123456789/23297.
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Dissertação (Mestrado em Tecnologia Nuclear)
IPEN/D
Instituto de Pesquisas Energeticas e Nucleares - IPEN-CNEN/SP
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Калашник, Наталія Володимирівна, Наталия Владимировна Калашник, Nataliia Volodymyrivna Kalashnyk, and А. А. Романовська. "Лактостаз тактика ведення та пріорітетні методи лікування." Thesis, Сумський державний університет, 2014. http://essuir.sumdu.edu.ua/handle/123456789/36489.
Full textAbstract:
Лактостаз – дисфункціональний стан лактуючої молочної залози, в основі якого лежить невідповідність процесів молокоутворення і молоковіддачі. Розвивається у породіль, які не годують молочними залозами і не зціджують їх або ж недотримуються правила грудного вигодовування за вимогою. Якщо лактостаз не купірується протягом 4–5 діб, в молочних протоках іде накопичення мікроорганізмів і розвивається мастит.
При цитуванні документа, використовуйте посилання http://essuir.sumdu.edu.ua/handle/123456789/36489
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Benítez, Sandra. "New insights into RANK signaling pathway in the mammary gland." Doctoral thesis, Universitat de Barcelona, 2021. http://hdl.handle.net/10803/673589.
Full textAbstract:
Receptor activator of nuclear factor kappa-β ligand (RANKL) and its receptor RANK are key mediators of bone resorption1,2. RANKL, its receptor RANK and its natural decoy receptor OPG, which is a competitive inhibitor that binds to RANKL and negatively regulates the pathway3, are members of the tumor necrosis factor (TNF) superfamily. Based on this key role in bone remodeling, a monoclonal antibody against RANKL, called denosumab, has been developed and is used in the clinics for the treatment of osteoporosis and bone metastasis. Moreover, RANK pathway is not only essential for bone remodeling, but also plays important roles in lymph node organogenesis, immune cell activation4,5 and mammary gland development6,7. Disrupted mammary gland development during pregnancy and impaired lactation are observed as a consequence of RANK loss or overexpression (under the MMTV-promoter)7,8. Defective alveologenesis in RANK-null mice has been attributed to decreased proliferation and survival of mammary epithelial cells6.
Overexpression of RANK in mammary epithelial cells enhances proliferation, impairs lactation and disrupts mammary cell fate resulting in the accumulation of MaSCs (mammary stem cells)9. Pharmacological inhibition of RANKL with RANK-Fc, which binds to RANKL and blocks the pathway, completely prevents MPA/DMBA-induced mammary tumor formation in WT mice. Thus, RANKL is the main mediator of the protumorigenic role of progesterone in the mouse mammary gland10. High levels of Rank in both mouse and human mammary epithelial cells (MECs) induce stemness and promote tumorigenesis and metastasis9,11. Conversely, inhibition of RANK pathway using genetic and pharmacological approaches decreases the incidence of spontaneous preneoplasic lesions, tumors and lung metastasis in the oncogene-driven MMTV-PyMT and MMTV-Neu mice10,12. Thus, inhibition of Rank signaling has emerged as a new strategy for breast cancer prevention and treatment.
Unexpectedly, we found a delayed latency in tumor formation and reduced tumor incidence in transgenic mice overexpressing in MECs both Rank and Neu or Rank and PyMT compared to single mutants. Despite the initial attenuation in tumor growth, Rank overexpressing tumors grew faster and seeded more lung metastasis, in agreement with an expansion of the cancer stem cell population. Mechanistically we found that Rank overexpression induced senescence in the mammary epithelia blocking the progression from hyperplasias to mammary intraepithelial neoplasia. High levels of senescence were observed in the mammary glands and cultured MECs of Rank transgenic mice, even in the absence of other oncogenic stimuli. Mice that overexpress Rank in the mammary gland are more susceptible to mammary
tumorigenesis driven by carcinogens and spontaneously develop mammary tumors after multiple pregnancies with long latency9,10. These results indicate that eventually Rank-overexpressing MECs evade or scape senescence allowing tumor formation. Moreover, infection of MECs and mouse embryonic fibroblast (MEFs) with Rank overexpressing vectors (but not PyMT or Neu) led to DNA damage and senescence. Like Ras, Rank induces a typical “oncogene-induced senescence (OIS)” through p16/p19. Senescence was also observed in the WT epithelia after Rankl exposure highlighting the physiological relevance of senescence during mammary gland development and tumor initiation. Importantly, Rank-OIS was essential for Rank-driven stemness, as the increased mammosphere forming ability of Rank overexpressing MECs and breast cancer cells is lost after senolytic treatments.
We uncovered an unexpected dual role for Rank in the mammary epithelia able to
induce stemness as well as OIS, delaying tumor initiation but increasing aggressiveness of established tumors once senescence is overcome.
Dougall WC, Glaccum M, Charrier K, et al. RANK is essential for osteoclast and lymph node development. Genes Dev. 1999;13(18):2412-2424. http://www.ncbi.nlm.nih.gov/pubmed/10500098. Accessed January 25, 2017.
2. Penninger JM, Kong Y-Y, Yoshida H, et al. OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node organogenesis. Nature. 1999;397(6717):315-323. doi:10.1038/16852
3. Dougall WC, Holen I, González Suárez E. Targeting RANKL in metastasis. Bonekey
Rep. 2014;3. doi:10.1038/bonekey.2014.14
4. Boyce BF, Xing L. Biology of RANK, RANKL, and osteoprotegerin. Arthritis Res
Ther. 2007;9(Suppl 1):S1. doi:10.1186/ar2165
5. Yasuda H, Shima N, Nakagawa N, et al. Osteoclast Differentiation Factor Is a Ligand for Osteoprotegerin Osteoclastogenesis-Inhibitory Factor and Is Identical to TRANCERANKL. Vol 95.; 1998. www.pnas.org. Accessed April 20, 2019.
6. Fata JE, Kong YY, Li J, et al. The osteoclast differentiation factor osteoprotegerin- ligand is essential for mammary gland development. Cell. 2000;103(1):41-50. http://www.ncbi.nlm.nih.gov/pubmed/11051546. Accessed January 25, 2017.
7. Gonzalez-Suarez E, Branstetter D, Armstrong A, Dinh H, Blumberg H, Dougall WC. RANK overexpression in transgenic mice with mouse mammary tumor virus promoter-controlled RANK increases proliferation and impairs alveolar differentiation in the mammary epithelia and disrupts lumen formation in cultured epithelial acini. Mol Cell Biol. 2007;27(4):1442-1454. doi:10.1128/MCB.01298-06
8. Cordero A, Pellegrini P, Sanz-Moreno A, et al. Rankl Impairs Lactogenic Differentiation Through Inhibition of the Prolactin/Stat5 Pathway at Midgestation. Stem Cells. 2016;34(4):1027-1039. doi:10.1002/stem.2271
9. Pellegrini P, Cordero A, Gallego MI, et al. Constitutive activation of RANK
disrupts mammary cell fate leading to tumorigenesis. Stem Cells.
2013;31(9):1954-1965. doi:10.1002/stem.1454
10. Gonzalez-Suarez E, Jacob AP, Jones J, et al. RANK ligand mediates progestin- induced mammary epithelial proliferation and carcinogenesis. Nature.
2010;468(7320):103-107. doi:10.1038/nature09495
11. Palafox M, Ferrer I, Pellegrini P, et al. RANK Induces Epithelial-Mesenchymal Transition and Stemness in Human Mammary Epithelial Cells and Promotes Tumorigenesis and Metastasis. Cancer Res. 2012;72(11):2879-2888. doi:10.1158/0008-5472.CAN-12-0044
12. Yoldi G, Pellegrini P, Trinidad EM, et al. Tumor and Stem Cell Biology RANK Signaling Blockade Reduces Breast Cancer Recurrence by Inducing Tumor Cell Differentiation. Cancer Res. 2016;76(19):1-13. doi:10.1158/0008-5472.CAN-15-
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Weber, Miriam S. "Overexpression of ovine insulin-like growth factor-I (IGF-I) in the mammary glands of transgenic mice." Thesis, This resource online, 1995. http://scholar.lib.vt.edu/theses/available/etd-05022009-040526/.
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Bielke, Wolfgang. "Identification snd characterization of programmed cell death-associated genes during involution of the mammary and prostate glands /." [S.l.] : [s.n.], 1994. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.
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Buser, Adam C. "Mechanism of progesterone receptor repression of transcription of the [beta]-casein gene in mammary epithelial cells /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2007.
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Thesis (Ph.D. in Cancer Biology) -- University of Colorado Denver, 2007.Typescript. Includes bibliographical references (leaves 182-210). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;
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Smith-Steinhart, Christine M. "TGF[beta] as a regulator of phagocytic competency in polarized mammary epithelial cells /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2007.
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Thesis (Ph.D. in Immunology) -- University of Colorado Denver, 2007.Typescript. Non-Latin script record Includes bibliographical references (181-196). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;
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Camba-Colón, Joanna Irene Rosa. "Role of the maternal liver in lactating mice." Diss., [Riverside, Calif.] : University of California, Riverside, 2010. http://proquest.umi.com/pqdweb?index=0&did=2019822721&SrchMode=1&sid=2&Fmt=2&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1274111729&clientId=48051.
Full textAbstract:
Thesis (Ph. D.)--University of California, Riverside, 2010.Includes abstract. Available via ProQuest Digital Dissertations. Title from first page of PDF file (viewed May 17, 2010). Includes bibliographical references. Also issued in print.
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Johnson, David W. "Regulation and site of action of exogenous and endogenous opioids on growth hormone and prolactin secretion in Holstein calves." Diss., Virginia Tech, 1990. http://hdl.handle.net/10919/39812.
Full textAbstract:
Four studies were conducted to investigate the effect and site of action of exogenous and endogenous opioids on pituitary growth hormone (GH) and prolactin (PRL) secretion in Holstein calves. In the first study, the effect of the opioid agonist DAMME (D-Ala²⁺,N-Me-Phe⁴,Met(O)⁵-01 enkephalin) on plasma GH and PRL secretion was measured in Holstein calves in fall season. Plasma concentrations of both GH and PRL increased in response to DAM ME injection. Pretreatment with either the lipid soluble opioid antagonist naloxone (NAL), which readily penetrates the blood brain barrier (BBB), or the peripherally acting antagonist methyl levallorphan mesiltate (MLM), blocked the PRL response to DAMME. Naloxone, but not MLM, negated the GH response to DAMME. In spring, the experiment was repeated with similar results.
In the second experiment, the opioid antagonists NAL and MLM were administered alone to detennine whether endogenous opioids mediate basal GH and PRL secretion, and the site of action of any of opioid-mediation of basal GH and PRL. In fall, NAL administration increased both plasma GH and PRL secretion. Methyl levallorphan mesilate did not affect PRL, but increased plasma GH concentrations. In spring, a second trial using 5 different doses of each antagonist was conducted. Naloxone did not affect GH levels at any dose in spring, but decreased plasma PRL at the same dose which increased plasma PRL in fall. Plasma PRL was again unaffected by MLM, but plasma GH was increased by 3 separate doses of MLM.
The third experiment was designed to determine if the increases in plasma PRL seen after DAMME administration were mediated via dopaminergic mechanisms. Plasma PRL in calves again increased in response to DAMME injection alone. In calves pre-treated with the long-acting dopamine agonist 2-Br-&alp. ergocryptine (CB 154), plasma PRL was unresponsive to DAMME injection. The pituitaries of calves treated with CB 154 in this experiment were able to respond to thyrotropin-releasing hormone (TRH) injection with increased PRL secretion.
In the final experiment, the role of growth hormone-releasing hormone (GRH) in facilitating GH release after DAMME injection was investigated, and whether endogenous opioidergic mechanisms play a role in mediating the effects of exogenous GRH on GH secretion. Plasma GH concentrations increased in calves receiving either DAMME or D-ala²⁺, fragment 1- 29 amide, a synthetic GRH. The immediate increase in plasma GH concentrations after GRH injection in calves pre-treated with DAMME was approximately 5 fold less than that in calves not pre- treated with DAMME. Calves receiving DAMME and GRH in combination also produced a GH response curve with greater area under it than either compound alone, indicating possible synergism between the synthetic GRH and a DAMME-sustained release of endogenous GRH. Naloxone administration concomitantly with synthetic GRH did not alter the ability of the synthetic GRH to increase GH secretion overall, compared to synthetic GRH alone.
In conclusion, these studies are the first to indicate that dairy breeds are able to respond to exogenous opioids with increased secretion of pituitary GH and PRL, as is known to occur in other mammalian species. Also, they indicate that opioid receptors mediating pituitary GH secretion to exogenous opioids in Holstein calves are located somewhere within the BBB, and those mediating PRL secretion are at a site outside the BBB. It appears from these studies that endogenous opioids within the BBB play a role in regulating basal PRL secretion, and that this regulation differs in fall and spring. A role for endogenous opioids in the regulation of GH secretion in Holstein calves may exist also, at least in fall, but the results are less conclusive. The peripheral opioid antagonist MLM alone may facilitate increased GH secretion in Holstein calves via an agonistic, not antagonistic, mechanism. These studies indicate that the increased PRL secretion seen following opioid administration in Holstein calves is mediated through a dopaminergic mechanism. It appears that endogenous opioids do not mediate the pituitary response to exogenous GRH in Holstein calves, and that GH increases after DAMME injection are facilitated, at least in part, by increased release of endogenous GRH.Ph. D.
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Романюк, Анатолій Миколайович, Анатолий Николаевич Романюк, Anatolii Mykolaiovych Romaniuk, Роман Андрійович Москаленко, Роман Андреевич Москаленко, Roman Andriiovych Moskalenko, and Г. В. Фреїва. "Вміст кальцію, заліза, міді, цинку в тканинах молочної залози при деяких формах її вогнищевої патології." Thesis, Вид-во СумДУ, 2005. http://essuir.sumdu.edu.ua/handle/123456789/6627.
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McFadden, Thomas Bernard. "Effects of feeding level and diet composition on mammary growth in prepubertal lambs and mice." Diss., Virginia Polytechnic Institute and State University, 1987. http://hdl.handle.net/10919/53636.
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Forty ewe lambs were grouped into four treatment groups: A) fed a standard, high-energy diet, ad libitum; G) fed as group A, but treated with GH (.1 mg/kg bodyweight/d); R) fed the standard diet in restricted amounts to a target weight gain of 120 g/d; S) fed a ration including 30% of a protected fat supplement, ad libitum. Rations were formulated to be isonitrogenous and isocaloric and were fed from approximately seven to 22 weeks of age. Growth rates differed in the order S>A = G> R, although final weights did not differ among ad libitum fed groups. Lambs in group S had heavier mammary glands, with greater amounts of parenchyma and fat pad and higher content of dry, fat-free parenchymal tissue compared to the mean of the remaining groups. Total gland weight was lower in group R, although weight of parenchyma was similar to groups A and G. Parenchyma made up a higher percent of total udder weight in lambs of group R compared to any other group. Parenchymal DNA content was not different by treatment, but glands from group G had twice the total DNA of groups A and R, and group S had 50% more than the latter groups. Volume of mammary glands occupied by parenchyma was increased by more than 50% in group S, compared to the other groups which were similar. Concentrations of prolactin receptors in mammary parenchyma and of GH receptors in liver were increased in lambs of group S. Percent Iinoleic acid in mammary parenchymal lipid of lambs in group S was increased relative to other groups. Unsaturated acids also made up a greater percentage of total fatty acids in group S. Feeding the protected fat supplement resulted in increased unsaturated fatty acid, especially linoleic acid, percentage in mammary fat. This effect was associated with increased mammary growth compared to lambs fed a standard ration. Lambs treated with GH showed some indications of increased mammary growth, but groups A and R were similar except for the increase in percent of gland occupied by parenchyma in group R.
In a second study, mammary growth in prepubertal mice increased with increasing dietary energy intake. Differences in ductal growth persisted at 18 weeks of age, and effects of exogenous steroids at this time were not significant. Prepubertal mammary growth in mice is not sensitive to inhibition by high plane of nutrition as is the case in ruminants.Ph. D.
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Wonsil, Brian John. "Influence of dietary fat and protein on nutrient supply and utilization by the lactating bovine mammary gland." Diss., Virginia Tech, 1993. http://hdl.handle.net/10919/38552.
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Chang, Cheng. "Function and Regulation of the α6 Integrins in Mammary Epithelial Biology and Breast Cancer: A Dissertation." eScholarship@UMMS, 2015. http://escholarship.umassmed.edu/gsbs_diss/734.
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Integrins have the ability to impact major aspects of epithelial biology including adhesion, migration, invasion, signaling and differentiation, as well as the formation and progression of cancer (Hynes 2002; Srichai and Zent 2010; Anderson et al. 2014). This thesis focuses on how integrins are regulated and function in the context of mammary epithelial biology and breast cancer with a specific focus on the α6 integrin heterodimers (α6β1 and α6β4). These integrins function primarily as receptors for the laminin family of extracellular matrix (ECM) proteins and they have been implicated in mammary gland biology and breast cancer (Friedrichs et al. 1995; Wewer et al. 1997; Mercurio et al. 2001; Margadant and Sonnenberg 2010; Muschler and Streuli 2010; Nistico et al. 2014).
The first project investigates how alternative splicing of the α6 subunit impacts the genesis and function of breast cancer stem cells (CSCs). This work revealed that the α6Bβ1 splice variant, but not α6Aβ1, is necessary for the function of breast CSCs because it activates the Hippo transducer TAZ (Zhao et al. 2008a), which is known to be essential for breast CSCs (Cordenonsi et al. 2011). My work also led to the discovery that laminin (LM) 511 is the specific ligand for α6Bβ1 and that autocrine LM511, which is mediated by TAZ, is needed to sustain breast CSCs by functioning as a ‘ECM niche’. An important aspect of this study is the finding that surface-bound LM511 characterizes a small population of cells in human breast tumors with CSC properties.
The second project of my thesis concentrated on identifying transcription factors that regulate expression of the β4 subunit. The expression of the α6β4 integrin is repressed during the epithelial-mesenchymal transition (EMT) (Yang et al. 2009) but the contribution of specific transcription factors to this repression is poorly understood. This study revealed that Snai1 is a transcriptional repressor of β4, which is responsible for establishing the PRC2 (Polycomb complex 2)- associated repressive histone mark H3K27Me3. However, I also found that the ability of Snai1 to repress transcription is abrogated by its interaction with Id2. Specifically, I identified the biochemical mechanism for how Id2 regulates Snai1. Id2 binds the SNAG domain of Snai1 that is the docking site for several corepressors (Peinado et al. 2004; Lin et al. 2010b; Dong et al. 2012a). One important consequence of Id2 interacting with Snai1 on the β4 promoter is that it prevents repressive epigenetic modifications. This finding may explain why some epithelial cells express Snai1 and β4 because they also express Id2 (Vincent et al. 2009; Bastea et al. 2012). The repression of the α6β4 integrin during the EMT is consistent with data indicating that this integrin is not expressed in CSCs (Mani et al. 2008; Goel et al. 2012; Goel et al. 2013; Goel et al. 2014). An important question going forward is to understand how the α6β4 integrin contributes to tumor formation.
In summary, my thesis provides novel insights into the biology of the α6 integrins that has important implications for the function of these integrins in mammary gland biology and breast cancer, especially our understanding of breast CSCs.
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Zeidan, Mohammad. "Assessment of Mean Glandular Dose in Mammography." Thesis, University of Canterbury. Department of Physics, 2009. http://hdl.handle.net/10092/2653.
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The mean glandular dose (MGD) was measured for a breast phantom by using molybdenum/molybdenum and molybdenum/rhodium target/filter combinations, at different kVp 26, 28 and 32 kilovolts. The phantom thickness was 7.5cm and was made of BR12 material. The change of dose was studied as a function of depth inside the phantom at different depths from the surface, namely 3.3, 4.3 and 5.3cm, by using TLDs. It was found that the MGD value for different combinations of beam quality (HVL) and energy (kVp) did not exceed the recommended values given by different protocols. The Mo/Rh target/filter required lower doses to achieve the same or better results compared with the Mo/Mo target/filter. The change in the surface dose as a function of kVp was more significant for Mo/Rh than for the Mo/Mo. Studying the change in dose within the breast, as a function of depth gives a better understanding of the interactions between radiation and tissue inside the breast. It should be noted that the MGD is a tool for optimization of the mammography parameters. However, the MGD should not be used directly to estimate the risk of determinable health effects from mammography. This will ultimately help to determine limits for the breast surface dose and a better understanding of cancer risk. In future work, we will try to measure the change of the dose as a function of depth by using more kVp, HVL, different breast composition and different target/filter combinations to give a wider picture for different situations.
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Mark, Thomas. "International genetic evaluations for udder health traits in dairy cattle /." Uppsala : Dept. of Animal Breeding and Genetics, Swedish University of Agricultural Sciences, 2005. http://epsilon.slu.se/200593.pdf.
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