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1

Ahn, Jae Suk. "Regulation of P2Y₂ nucleotide receptor expression in salivary glands." free to MU campus, to others for purchase, 2001. http://wwwlib.umi.com/cr/mo/fullcit?p3012944.

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2

Llupi, Matilda, and Rabije Qoku. "Expression of mucins in normal salivary glands and mucoepidermoid carcinoma of salivary glands." Thesis, Malmö högskola, Odontologiska fakulteten (OD), 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:mau:diva-19760.

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Mucoepidermoid carcinom (MEC) är en malign mucin-producerande tumör som förekommer i både stora och små spottkörtlar. Syftet med denna studie var att undersöka histologiskt uttryck av muciner (MUC1, MUC4, MUC5AC, MUC5B, MUC6) i MEC för att eventuellt hitta en korrelation mellan kvalitativt mucinuttryck och tumörgrad. Tolv låg- och fem höggradiga MEC och nio normala spottkörtlar intill tumörvävnad undersöktes med hjälp av immunohistokemi där proverna utvärderades med avseende på färgningsmönster och positivitet i specifika celltyper. Normala spottkörtelceller uttryckte främst cytoplasmatiskt mucin MUC5B. MUC1 och MUC4 uttrycktes i normala spottkörtelgångsceller i ungefär hälften av proverna medan MUC5AC uttryck var sällsynt i normala spottkörtlar. MEC:ar uttryckte MUC1, MUC4, MUC5AC och MUC5B. Den apikala delen av membranet i de bägarceller som omger cystiska hålrum visade den starkaste färgningen för MUC1 och MUC4. Uttryck av MUC4 i bägarceller minskade med ökad histologisk grad. Bägarcellers uttryck av MUC5B:s i låggradig MEC var mindre intensivt än uttrycket av MUC5AC i samma celler. Högre uttryck av MUC5B jämfört med MUC5AC noterades i höggradiga tumörer. Sammanfattningsvis uttrycker MEC olika mängd av muciner än normala spottkörtlar. MUC5AC:s uttryck i MEC verkar vara en metaplastisk funktion och MUC4 tycks relatera till tumörens differentieringsgrad. Förhållandet mellan MUC5AC och MUC5B uttryck skulle kunna vara ett användbart verktyg vid diagnostisering och prognosutvärdering av MEC.
Mucoepidermoid carcinomas (MECs) are malignant epithelial mucin-producing tumours encountered in both major and minor salivary glands. The aim of this study was to investigate the histological characteristics of the expression of mucins (MUC1, MUC4, MUC5AC, MUC5B, MUC6) in MECs in search for a possible correlation between qualitative mucin expression and tumour grade. Twelve low-grade, five high-grade MECs and nine normal salivary glands adjacent to tumour tissue were investigated for these mucins by immunohistochemistry. The samples were evaluated with respect to staining pattern and positivity of specific cell types. Normal acinar cells mainly expressed the cytoplasmic mucin MUC5B. MUC1 and MUC4 were expressed in normal ductal cells in approximately half of the samples whereas MUC5AC expression was rare in normal salivary glands. MECs expressed MUC1, MUC4, MUC5AC and MUC5B. The apical membrane of mucous cells lining the cystic cavities showed the strongest staining for MUC1 and MUC4. The expression of MUC4 in mucous cells decreased with increasing histological grade. Expression of salivary mucin MUC5B in mucous cells in low-grade MECs was less intense compared to the expression of MUC5AC in the same cells. In high-grade tumours, a higher expression of MUC5B compared to MUC5AC was noted. In conclusion, MECs express different mucin quantity compared to normal salivary glands. MUC5AC expression in salivary tumour tissue seems to be a metaplastic feature and MUC4 appears to be related to tumour differentiation grade. The relationship between MUC5AC and MUC5B expression could be a useful tool in the diagnosis and estimation of prognosis of MECs.
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3

Bourdon, David M. "Serotonin receptors in mammalian salivary glands." free to MU campus, to others for purchase, 2001. http://wwwlib.umi.com/cr/mo/fullcit?p3012950.

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4

Dallal, Nadeem D. McArthur Carole. "An investigation of HIV in Cameroon exploring the link between risk-taking behavior, salivary hormones and AIDS; and delineating the effect of HIV-1-TAT on human salivary gland cells in an in vitro model of diffuse infiltrative lymphocytosis syndrome /." Diss., UMK access, 2004.

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Thesis (M.S.)--School of Dentistry. University of Missouri--Kansas City, 2004.
"A thesis in oral biology." Typescript. Advisor: Carole McArthur. Vita. Title from "catalog record" of the print edition Description based on contents viewed Feb. 23, 2006. Includes bibliographical references (leaves 83-91 ). Online version of the print edition.
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5

Newey, Paul J. "The role of the tumour suppressor proteins, parafibromin and menin, in endocrine tumourigenesis." Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.711613.

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6

Dunér-Engström, Marianne. "On the role of peptides and classical transmitters in the regulation of salivary glands." Stockholm : Karolinska Institutet, 1993. http://catalog.hathitrust.org/api/volumes/oclc/29572365.html.

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7

Luts, Lena. "Neurohormonal modulators in the parathyroid gland localization and regulation /." Lund : Dept. of Physiology and Neuroscience, Section of Neuroendocrine Cell Biology, University of Lund, 1997. http://catalog.hathitrust.org/api/volumes/oclc/38987917.html.

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8

Sagulin, Gun-Britt. "Effects of calcium and calciotropic hormones on salivary gland function." Stockholm : Kongl. Carolinska Medico Chirurgiska Institutet, 1989. http://catalog.hathitrust.org/api/volumes/oclc/20620549.html.

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9

Ustenko, R. L., N. L. Svintsitska, and A. A. Kobets. "Three-dimenional organization of the glands of peripheral zone of the human prostate gland." Thesis, Сумський державний університет, 2013. http://essuir.sumdu.edu.ua/handle/123456789/31893.

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The work is a fragment of the Higher State Educational Establishment of Ukraine «Ukrainian medical stomatological academy». The name of the research work is a «Structural and three-dimensional organization of the exocrine glands and organs of the human digestive tract in healthy and people patients». When you are citing the document, use the following link http://essuir.sumdu.edu.ua/handle/123456789/31893
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10

Van, Wyk Elizabeth Joy. "Pineal-adrenal gland interactions in search of an anti-stressogenic role for melatonin." Thesis, Rhodes University, 1993. http://hdl.handle.net/10962/d1004115.

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The multiple functions of the pineal gland have been collectively interpreted as constituting a general anti-stressogenic role. The adrenal glands play a central role in maintaining homeostasis. The major neuroendocrine consequence of long-term stress is elevated circulating glucocorticoid levels. In this study, the effect of chronic, oral hydrocortisone treatment on pineal biochemistry was investigated in male Wi star rats of the albino strain. The results show that seven days of oral hydrocortisone treatment endows the pineal gland with the ability to increase melatonin synthesis in organ culture. The increase is accompanied by a rise in NAT activity, cyclic AMP levels and enhanced specific binding to the pineal B-adrenergic receptors. It appears that hydrocortisone sensitizes the pineal gland to stimulation by B-adrenergic agonists. thus rendering the pineal more responsive to B-adrenergic agonists. Further studies were directed at demonstrating an anti-stressogenic function for the pineal gland by investigating whether the principal pineal indole, melatonin. could protect against the deleterious effects of elevated. circulating drocortisone levels. The results show that chronic, oral hydrocortisone treatment significantly increases liver tryptophan pyrrolase activity. The catabolism of tryptophan by tryptophan pyrrolase is an important determinant of tryptophan availability to the brain, and therefore, brain serotonin levels. The findings show that melatonin inhibits basal and hydrocortisone-stimulated liver tryptophan pyrrolase apoenzyme activity in a dose-dependent manner. This inhibition suggests that melatonin may protect against excessive loss of tryptophan from circulation and against deficiencies in the cerebral serotinergic system which are associated with mood and behavioural disorders. It was shown that another deleterious effect of chronic hydrocortisone treatment is a significant increase in the number of glutamate receptors in the forebrain of male Wistar rats. The increase in receptor number observed in this study is probably due to an increase in the synthesis of glutamate receptors and is associated with a marked reduction in the affinity of the glutamate receptors for glutamate. possible to demonstrate an receptor number or the For practical reasons, it was not effect of melatonin on either glutamate affinity of glutamate receptors for glutamate in rat forebrain membranes. In view of the neurotoxic effect of glutamate in the eNS, the functional significance of recently described glutamate receptors in the pineal gland was investigated. The results show that 10-4 M glutamate significantly inhibits the isoprenaline-stimulated synthesis of N-acetylserotonin and melatonin in organ culture when the pineal glands were pre-incubated with glutamate for 4 hours prior to stimulation with isoprenalin and when glutamate and isoprenaline were administered together in vitro. GABA, a glutamate metabolite could not mimic the decrease in isoprenalinestimulated melatonin, and it is likely that the observed effects were directly attributed to glutamate. Incubation of the pineal gland with 10-4 M glutamate in organ culture did not affect HIOMT activity in pineal homogenates, but significantly elevated both basal and isoprenaline-stimulated NAT activity. It was concluded that glutamate only inhibits melatonin synthesis in intact pineal glands and not in pineal homogenates. The present study has provided further support for an interaction between the pineal and the adrenal glands. There is an ever increasing likelihood that melatonin is an anti-stressogenic hormone and that the pineal gland may have a protective role to play in the pathology of stress-related diseases.
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11

Lessey, Andrew James. "The role of C-type natriuretic peptides (CNP) on pituitary development and body growth in zebrafish : molecular investigations of neuroendocrine development." Thesis, Royal Veterinary College (University of London), 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.701675.

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12

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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13

Dwyer, Virginia Michelle Gregory 1955. "A STUDY OF PINEAL GLAND POLYPEPTIDES AND PROTEINS BY POLYACRYLAMIDE GEL ISOELECTRIC FOCUSING (PAG-IEF) AND TWO-DIMENSIONAL ELECTROPHORESIS (2DE) (BRAIN REGIONS)." Thesis, The University of Arizona, 1986. http://hdl.handle.net/10150/276560.

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14

Morris, Andrew Paul. "The electrophysiology of mammalian salivary glands." Thesis, University of Liverpool, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279746.

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15

Ali, Mahmoud Fadl. "Chemical investigations of insect exocrine glands." Thesis, Keele University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.328532.

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16

Bourdon, David Milon. "Serotonin receptors in mammalian salivary glands /." free to MU campus, to others for purchase, 2001. http://wwwlib.umi.com/cr/mo/fullcit?p3012950.

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17

Çevik, Aras Hülya. "Secretory and anti-inflammatory actions of some gastro-intestinal hormones in salivary glands /." Göteborg : Institute of Neuroscience and Physiology, Section of Pharmacology, The Sahlgrenska Academy at Gothenburg University, 2009. http://hdl.handle.net/2077/20460.

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18

Li, Liang. "Regulation of phospholipase D in submandibular glands." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0018/NQ53062.pdf.

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19

Franzén, Lars. "Effects of fractionated irradiation on salivary glands." Doctoral thesis, Umeå universitet, Onkologi, 1992. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-101770.

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The thesis is a study of the effects of radiation on the salivary glands in an experimental and a clinical study. Irradiation is a cornerstone in the management of head and neck cancer and is as other modalities of cancer treatment, afflicted with adverse reactions. An optimal radiotherapy regime is limited by the sensitivity of the normal tissues with regard to early and late effects. In certain cases the early effects can be so troublesome that it will cause interruption in the irradiation and questioning of the curative intention. Although DNA is the lethal target, other parts of the cell have been proposed as sensitive targets to irradiation. Different in vitro secretory models and quantitative morphological characterization and immunohistochemical evaluation of neuropeptides were performed in rat salivary glands after irradiation. The irradiation was given unilaterally or bilaterally once a day for a five-day schedule with 6 MV photons (total dose 20, 30, 35, 40, 45 Gy) or a two fractions regime in five days with a total dose of 24 or 32 Gy. The contralateral gland served as a control for unilaterally treated animals and parallel analyses were done 10 days or 180 days following the last irradiation dose. An early, dose-dependent effect of fractionated irradiation on noradrenaline-stimulated potassium fluxes (86Rb+ fluxes) was demonstrated. In contrast, the exocytotic amylase release displayed no obvious alterations, and morphologically no changes were seen. Regarding late effects (180 days) the noradrenaline-stimulated electrolyte secretion was decreased at least for the higher doses of irradiation. Amylase content and loss of acini was also dose-dependently decreased. At 10 days after bilateral irradiation there was a marked increase in the expression of the neuropeptides substance P, leu-enkephalin and bombesin in the ganglionic cells associated with the submandibular glands and in nerve fibers of the glandular parenchyme. In addition, a clinical prospective evaluation of 25 patients was performed before, during radiotherapy and 6, 12 and 18 months after the end of treatment. A great interindividual variation in the recovery was demonstrated with regard to salivary flow rate. Irradiation doses about 40-50 Gy caused generally reversible changes; sometimes salivary secretion was almost completely restored 6-18 months after the end of radiotherapy. Doses exceeding 65 Gy induced almost irreversible alterations. Even if DNA is the target for the lethal effect of irradiation, other constituents, such as the cell membrane or neuropeptide expression can be significantly affected by irradiation and cause important physiological changes.

S. 1-43: sammanfattning, s. 47-164: 6 uppsatser


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20

Sanderson, Christopher Mark. "Transport of IgA in rat salivary glands." Thesis, University of Surrey, 1986. http://epubs.surrey.ac.uk/847984/.

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Transport of polymeric immunoglobulin A (plgA) in rat salivary glands has been investigated by combined morphological and biochemical techniques in vivo and in vitro. The distribution of IgA and its cellular receptor secretory component (SC) was observed by immunoperoxidase staining of cryosections from parotid and submaxillary gland, showing serous acinar cells are the site of IgA transport into saliva. Binding of horse radish peroxidase specific IgA to parotid serous acinar cells in vitro, observed by electron microscopy, shows that only the basolateral domain of acinar cells possesses exposed SC. A combination of new cell fractionation methods and standard western blotting techniques shows that SC present on basolateral plasma membrane of parotid acinar cells has a molecular weight (mwt) >100,000 and shows a high affinity for plgA in vitro. The existence of a 73,000 mwt SC occurring with plgA in cellular fractions of parotid gland suggest cleavage of SC occurs prior to secretion. The kinetics of plgA trancytosis was studied using isolated parotid acini. Bound plgA was secreted into the incubation medium as slgA, within thirty minutes of incubation at 37°C. Secretion of plgA was initially rapid but slowed over a 2hr period of incubation at 37°C. In addition to facilitating plgA transport serous acinar cells also synthesise and secrete a diverse range of other salivary proteins which are packaged into secretion granules and secreted directly through the apical plasma membrane. It is improbable that one complex secretory pathway facilitates both bulk secretion of salivary protein and transport of plgA. Therefore secreted proteins must be selectively segregated during secretion into saliva. Secretion of proteins from acinar cells in vitro shows proteins are released at two distinct rates.
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21

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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22

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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23

Tobin, Gunnar. "Neuropeptides and atropine-resistant parasympathetic responses in salivary glands an experimental study in ferrets and some other species /." Lund, Sweden : Dept. of Physiology and Biophysics, Lund University, 1991. http://books.google.com/books?id=WaZpAAAAMAAJ.

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24

Ter-Antonyan, Vardan. "Iontophoretic trans-dermal drug delivery through sweat glands." [Tampa, Fla.] : University of South Florida, 2005. http://purl.fcla.edu/fcla/etd/SFE0001209.

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25

Kasaian, Katayoon. "Genomic analysis of head and neck endocrine glands." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/54936.

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Discovering biomarkers and molecular drivers of head and neck endocrine tumors was the inspiration for this thesis. Here, I describe the molecular evaluation of tumors of the thyroid and parathyroid endocrine glands for the purpose of identifying somatic driver alterations in these cancers. While molecular interplay of the germline genomic background of an individual and the somatic genome that emerges throughout the lifetime plays significant roles in increasing the susceptibility to cancer and in driving the malignant phenotype, the major known contributors to cancer remain the acquired somatic mutations. Analysis of a sporadic and recurring parathyroid carcinoma, with incidence of 1 per million population, revealed mutations in mTOR, MLL2, CDKN2C and PIK3CA and comparison of patient-matched primary and recurrent malignant tumors uncovered loss of PIK3CA activating mutation during the evolution of the tumor. Loss of the short arm of chromosome 1 along with somatic missense and truncating mutations in CDKN2C and THRAP3 provided new evidence for the potential role of these as tumor suppressors. Hürthle cell thyroid carcinoma accounts for a small proportion of all thyroid cancers; however, this malignancy often presents at an advanced stage and poses unique challenges. Genomic analysis revealed large regions of copy number variation encompassing nearly the entire genomes accompanied also by near haploidization. Moreover, I identified loss-of-function mutations of the tumor suppressor gene MEN1 in 4% of patients. Repeated alterations of the epigenetic machinery in anaplastic thyroid carcinoma, one of the most fatal of all adult solid malignancies, and novel gene fusions including MKRN1-BRAF, FGFR2-OGDH and SS18-SLC5A11 are reported here. The transcriptomic analysis suggested known drug targets such as FGFRs, VEGFRs, KIT and RET to have low expressions in this cancer; however, through integrative data analysis, I identified the mTOR signaling pathway as a potential therapeutic target for anaplastic thyroid cancer. Molecular analysis of papillary thyroid carcinoma and benign thyroid nodules revealed very low mutation rates in these tumors with CYP1B1, PTPRE, CTSH and RUNX1 emerging as promising diagnostic markers. The key somatic mutations identified in these studies can serve as novel diagnostic markers as well as therapeutic targets.
Science, Faculty of
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26

Välimäki, Stiina. "Growth of parathyroid glands : genetic and functional aspects /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-704-5.

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27

Xie, Weiliang. "Regulators of airway submucosal glands development and functions." Diss., University of Iowa, 2012. https://ir.uiowa.edu/etd/3409.

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Tracheobronchial submucosal glands (SMGs) develop from clusters of epithelial progenitor cells basally orientated within the surface airway epithelium called primordial glandular placodes (PGPs). Signal transduction events that coordinate the transitional process from PGPs into fully developed SMGs consisting of intricately branched networks of tubular secretary structures are still poorly understood. Wnt/β-catenin dependent induction of lymphoid enhancing factor-1 (Lef-1) expression in PGP progenitor/stem cells is required for SMG formation and maturation in the airway. In an effort to better understand the regulatory mechanisms that control Lef-1 during airway SMG development, I have studied its transcriptional regulation. I discovered that Sox2 expression is predominantly confined to the surface airway epithelium (SAE) and is repressed as Lef-1 is induced within PGPs. Deletion of Sox2 in polarized primary airway epithelia significantly enhances Lef-1 mRNA expression. Consequently, my hypothesis is that Sox2 functions as a negative regulator of Lef-1 expression in the SAE. I demonstrated that Sox2 modulates the expression of Lef-1 both independent and dependent on Wnt/β-catenin signaling. I discovered that a Sox2-binding site located in the Wnt Responsive Element (WRE) region of the 2.5Kb Lef-1 promoter is required for Sox2-mediated inhibition of β-catenin-dependent Lef-1 promoter transcription. It is important to understand the biology of SMG development because SMGs are the major mucus-producing structures in the proximal airway and are important in regulating the innate immunity of the lung in response to various neural signals. SMG ducts have also been proposed as a potential protective niche for slowly cycling progenitor cells (SCPCs). Hence, aberrant SMG function is thought to aggravate the pathoprogression of lung disease. Cystic fibrosis (CF) is a disease caused by a defect in the gene that encodes a chloride ion channel called cystic fibrosis transmembrane conductance regulator (CFTR). The absence of CFTR in serous cells within SMG ducts contributes to defective airway secretion, which alters the microenvironment within SMGs. I hypothesized that the glandular SCPC niche may be dysfunctional in CF. I reported that the neural peptide, calcitonin gene-related peptide (CGRP) activates CFTR-dependent SMG secretions and that this signaling pathway is hyperactivated in CF human, pig, ferret, and mouse SMGs. CFTR-deficient mice failed to maintain glandular SCPCs following airway injury, suggesting that the glandular SCPC niche may be dysfunctional in CF. CGRP levels increase following airway injury and function as an injury-inducible mitogen that stimulates progenitor cell proliferation. However, components of the receptor for CGRP (RAMP1 and CLR) were expressed in a very small subset of SCPCs, suggesting that CGRP indirectly stimulates SCPC proliferation through paracrine mechanisms. This discovery may have important implications for injury/repair mechanisms in the CF airway.
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Larsson, Olof. "Peptides as cotransmitters in salivary secretion histochemical, biochemical and functional studies of parotid and submandibular glands /." Stockholm : Kongl. Carolinska Medico Chirurgiska Institutet, 1989. http://catalog.hathitrust.org/api/volumes/oclc/19412146.html.

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29

Park, Minjung Kang. "P2 nucleotide receptors during postnatal development of rat salivary glands." free to MU campus, to others for purchase, 1999. http://wwwlib.umi.com/cr/mo/fullcit?p9946285.

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30

Lombaert, Isabelle Madeleine Armand. "Regeneration of irradiated salivary glands by stem cell therapy." [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 2008. http://irs.ub.rug.nl/ppn//.

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31

Lindsay, Susan L. "P2Y receptors in human sweat glands : localisation and function." Thesis, Glasgow Caledonian University, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404652.

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32

Jackson, Brian Derek. "Chemical studies of volatiles from exocrine glands of ants." Thesis, Keele University, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306866.

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Kawashima, Naomasa. "The interaction of mTOR and autophagy in salivary glands." Thesis, King's College London (University of London), 2018. https://kclpure.kcl.ac.uk/portal/en/theses/the-interaction-of-mtor-and-autophagy-in-salivary-glands(a5382fc9-c83b-4046-bff4-98c1b4ed91c5).html.

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Radiation therapy to treat head and neck cancer damages salivary glands, leading to decreased salivary flow which can cause xerostomia (perception of dry mouth), mucositis and dysphagia. These symptoms of salivary gland hypofunction are a major cause of patients stopping their treatment and greatly decrease their quality of life after treatment. Protecting from damage is essential to avoid these problems so this thesis examined some of the damage mechanisms present in salivary glands. Two intracellular processes seem to be particularly relevant. Mammalian Target of Rapamycin (mTOR) is a growth pathway often activated in cancers, repair and regeneration whereas autophagy is a self-digestion of cellular contents often associated with damage that helps to protect cells from apoptosis. Normally the two processes are linked by an enzyme UNC-like kinase (ULK) in a mutually exclusive way so that growth and degradation do not occur at the same time. However, both mTOR and autophagy have been shown to have beneficial effects after irradiation. Therefore, we decided to study the interactions between mTOR and autophagy in order to find an efficient way to uncouple mTOR and autophagy to protect irradiated salivary glands. Since ULK was an important link between mTOR and autophagy, an interesting new ULK inhibitor MRT67307 was used on salivary glands. In the first part of this study, we evaluated the effects of MRT67307 on cell cultures in order to collect enough data before trying the drug in vivo. Initially NIH 3T3 cells, a well-studied cell model, were cultured to verify the effects of MRT67307. As previously reported, the drug blocked starvation- and Torin 1 (an mTOR inhibitor)- induced autophagy. The next step was to test the effects of the drug on salivary acinar cells which were known to be very sensitive to irradiation. SMG-C6 cells were chosen since they were previously derived from rat submandibular acinar cells. In these cells, in contrast to NIH 3T3 cells, Torin 1 failed to upregulate autophagy, suggesting that mTOR and autophagy were not linked by ULK. This finding was interesting and novel and was further tested in primary-cultured cells (ie in vitro) from mouse submandibular glands. Again, administration of Torin 1 inhibited mTOR but did not activate autophagy and MRT67307 had no effect on marker of autophagy (LC3-I/LC3-II ratios). It could be inferred from these experiments that MRT67307 is a useful tool in examining mTOR/autophagy interactions through ULK1 and that in salivary glands autophagy and mTOR could be activated simultaneously. In the second part of this study, we carried out whole body irradiation of mice to study damage, mTOR-autophagy interactions and saliva flow variation in irradiated salivary glands. A dose escalation study appeared to cause minimal damage to salivary glands when the maximum dose of 11 Gy was given. To determine if salivary hypofunction had occurred whole mouth saliva was collected under temporary gaseous anaesthesia by the administration of pilocarpine (I.P.). Surprisingly, despite minimal histological indications of damage an increase in salivary function occurred. Biochemical analyses of the salivary glands indicated autophagy was transiently and weakly activated a few hours after irradiation whereas mTOR activity occurred a few days later. The use of a whole body irradiator limited the dose of irradiation to the salivary glands. Thus as a model system, transient mTOR activation probably had a beneficial effect, since pilocarpine stimulated saliva flow experiment showed a transient increase of saliva flow. However, this model system did not yield the expected salivary gland damage seen in other studies so instead another model of salivary gland damage, ductal ligation was studied. The third part of this study attempted to use autophagy-inhibitors in vivo, using the ligated salivary gland since autophagy activation was weak and did not last in irradiated salivary gland. Whole body injection of autophagy inhibitors chloroquine and MRT67307 (at two different doses and injection intervals) did not appear to have any beneficial effect on submandibular glands, except a slight delay of atrophy in both chloroquine and MRT67307 treated glands. Autophagy appeared to be mainly mTOR independent since MRT67307 failed to inhibit autophagy. This thesis contains novel data to indicate that autophagy and mTOR are independent of each in mouse submandibular glands. To the best of our knowledge, this is the first time that MRT67307 was used in vivo and no paper demonstrates an mTOR independent activation of autophagy in salivary glands. It provides the basis for further studies to protect salivary glands from irradiation damage by upregulating both mTOR and autophagy simultaneously, something that has not, so far, been tested.
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34

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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35

Rigby, Lawrence Dale. "Of goat glands, potency pills, and other conjugal acts /." free to MU campus, to others for purchase, 2000. http://wwwlib.umi.com/cr/mo/fullcit?p9988695.

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36

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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37

Yuk-lun, Kam. "The efficacy of a novel lubricating system in the management of radiotherapy related xerostomia." Click to view the E-thesis via HKUTO, 2004. http://sunzi.lib.hku.hk/hkuto/record/B31981835.

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38

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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39

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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40

Jacobsson, Gunilla. "Proteins regulating vesicular docking and fusion : histochemical studies on their presence and regulation in endocrine, neuroendocrine and neuronal cells /." Stockholm, 1997. http://diss.kib.ki.se/1997/91-628-2775-8.

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41

Yuan, Shi-Zeng. "Hypoxia and autoresuscitation in the neonatal rodent : with special reference to the sympatho-adrenal system /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3359-6.

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42

Otto, Gregory M. "Gustatory sweating after parotid surgery /." Title page, contents and abstract only, 1987. http://web4.library.adelaide.edu.au/theses/09MS/09ms091.pdf.

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43

Debono, Miguel. "Defining glucocorticoid status and normalising cortisol levels in adrenal disease." Thesis, University of Sheffield, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.632549.

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44

盧寵猷 and Chung-yau Lo. "Optimizing parathyroid autotransplantation during thyroidectomy." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B30257463.

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45

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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46

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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47

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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48

Castillo-Ronquillo, Yasmyne S. "The mechanisms of malignant transformation in benign salivary gland tumors /." Connect to full text in OhioLINK ETD Center, 2009. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=toledo1250207420.

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Thesis (M.S.)--University of Toledo, 2009.
Typescript. "Submitted as partial fulfillment of the requirements for the Master of Science in Biology." "A thesis entitled"--at head of title. Bibliography: leaves 54-65.
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49

Lo, Chung-yau. "Optimizing parathyroid autotransplantation during thyroidectomy /." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B22190132.

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50

Go, Yin-yin. "Quantitative structural studies of neoplasms of the parotid gland /." Hong Kong : University of Hong Kong, 1995. http://sunzi.lib.hku.hk/hkuto/record.jsp?B1403492X.

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