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Rozprawy doktorskie na temat „Up-regulation”

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Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 10 marca 2023

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1

Schrader-Ratchford, Ann Marie. "P2Y₂ nucleotide receptor up-regulation and function in submandibular gland epithelium". Diss., Columbia, Mo. : University of Missouri-Columbia, 2005. http://hdl.handle.net/10355/4189.

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Thesis (Ph. D.)--University of Missouri-Columbia, 2005.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "May 2005" Includes bibliographical references.
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2

Swan, Edward. "The legal development of derivatives trading and regulation up to 1848". Thesis, University of London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300756.

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3

McColgan, Peter. "Structural brain network degeneration and functional up-regulation in Huntington's disease". Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10041942/.

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Huntington’s disease (HD) is a neurodegenerative disorder caused by a CAG repeat expansion in the Huntingtin gene on chromosome 4. In recent years there have been significant advances in understanding both the cellular pathology and the macrostructural changes that occur in the striatum and cortical structures as the disease proceeds. However, it remains unclear how abnormalities at the cellular level lead to characteristic patterns of macrostructural change in the brains of HD patients. In this thesis I aim to link structural and functional brain network abnormalities with regional changes at the cellular level. Using diffusion tractography and resting state functional MRI in well characterised HD cohorts I examine the relationship between structural and functional brain network organisation. I link these changes in structure and function to the neuropsychiatric symptoms prevalent in HD, occurring years before the manifestation of motor symptoms. By characterising changes in white matter brain networks I reveal how the brain network breaks down as HD progresses and show how this network deterioration leads to the emergence of clinical deficits. Using characteristics of the healthy white matter brain network I demonstrate how it is possible to predict the atrophy of specific brain connections in HD over time. In doing so I highlight a hierarchy of white matter connection vulnerability showing cortico-striatal connections are the first to be affected. In order to link these macrostructural white matter changes to cellular level abnormalities I utilise data from the Allen Institute transcription atlas and show how differences in regional gene expression in the healthy brain can account for the selective vulnerability of specific white matter connections in HD. The work presented in this thesis demonstrates how linking systems and cellular pathobiology in HD can inform us about disease mechanisms that drive brain atrophy and ultimately lead to clinical deficits.
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4

Li, Yu-Hsuan. "Competitiveness in Power System Frequency Regulation Markets : Competitive analysis of the FCR-D up regulation market in Sweden". Thesis, KTH, Energiteknik, 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-300745.

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The growing share of weather-dependent power generation in the Swedish power system is challenging the stability of the whole system. Therefore, the need to increase system flexibility by frequency regulation reserves is enlarged. Nowadays, the reserves are mainly supplied by Hydropower. The TSO, Svenska kraftnät, is opening the market to attract new participants to provide the balancing capacity to increase the competition between resources and change the market dynamics. This thesis explores the potential of four different technologies in the future FCR-D upregulation market: Hydropower, Wind power, battery energy storage systems (BESS) and demand response (DR). A FCR-D upregulation market-clearing model has been built with logical cost calculation and volume estimation of each actor in the FCR-D market. Sensitivity analysis and the market-clearing model have been conducted through Python software. Based on the scenario selection method, this research provides an overview of the future FCR-D upregulation market with the participation of new actors. The results show that the availability for FCR-D up market of some Hydropower actors has decreased over the years. The Wind power has the highest cost among the studied technologies and the costs of the BESS and DR are competitive. Besides, in high spot price years, the bids from BESS and DR have higher chance to be accepted which creates opportunities to attract new actors to join the market. The new actors' introduction could lower the average FCR-D clearing prices from 19.3 - 70.7 % from 2016 - 2020. Finally, from the volume change scenario, the BESS and DR actors are found to be the price-makers that could influence the FCR-D price with rising available volume.
Den växande andelen väderberoende kraftproduktion i det svenska elsystemet utmanar stabiliteten i hela systemet. Därför växer behovet av att öka systemflexibiliteten genom än mer frekvensregleringsresurser. Numera hanteras frekvensreglering främst av vattenkraft, men Svenska kraftnät (Sveriges systemoperatör), öppnar marknaden alltmer för att locka nya deltagare, för att ge mer balanseringskapacitet och för att öka konkurrensen mellan resurser samt för att förstärka marknadsdynamiken. Detta examensarbete undersöker potentialen för fyra olika tekniker för den framtida stödtjänsten uppreglering för frekvenshållningsreserv för störd drift (FCR-D): vattenkraft, vindkraft, batterilagringssystem och laststyrning (konsumtionsminskning). En modell för klarering av FCR-D uppreglering har byggts upp med logisk kostnadsberäkning och volymuppskattning för varje aktör på FCR-D-marknaden. Känslighetsanalys och marknadsklarerings-modellen har genomförts i Python-programvara. Baserat på scenarievalsmetoden ger denna forskning en överblick över den potentiella framtida FCR-D uppregleringsmarknaden med deltagande av nya aktörer. Resultaten visar att tillgängligheten för FCR-D-marknaden för vissa vattenkraftaktörer har minskat genom åren. Vindkraften har den högsta kostnaden bland de studerade teknikerna medan kostnaderna för batterilagringssystem och laststyrning är konkurrenskraftiga. Dessutom har buden från batterilagringssystem och laststyrning under perioder med höga spotpriser större chans att bli accepterade, vilket skapar möjligheter att locka nya aktörer att gå med på marknaden. De nya aktörernas entré kunde ha sänkt genomsnittliga FCR-D klareringspriser med 19,3 till 70,7 % för perioden 2016 till 2020. Slutligen visar volymändringsscenariot att batterilagringssystem och laststyrning -aktörerna kan påverka FCR-D-priset med stigande tillgänglig volym.
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5

Shen, Jianzhong. "Purinergic proliferation of coronary smooth muscle : receptor cloning, up-regulation and signaling /". Free to MU Campus, others may purchase, 2005. http://wwwlib.umi.com/cr/mo/fullcit?p3204628.

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6

Mohd, Imran Kamalliawati. "Up-regulation of Hedgehog signalling in satellite cells and skeletal muscle regeneration". Thesis, University of Sheffield, 2019. http://etheses.whiterose.ac.uk/22909/.

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About half of the human body mass is comprised of skeletal muscles, a component of the musculoskeletal system involved in maintaining body posture, gait and locomotion. Additionally, skeletal muscles have essential function in glucose metabolism and thermoregulation. Thus, maintenance of skeletal muscle homeostasis is critical for the health of organisms. Satellite cells are muscle-specific stem cells responsible for postnatal growth, regeneration upon injury, and maintenance of skeletal muscle homeostasis. Satellite cell's activity is regulated by a sophisticated network of signalling pathways, which act in a combinatorial manner to regulate satellite cell expansion and differentiation, and to preserve a pool of stem cells during the life course of skeletal muscles. Many of these signalling pathways are known to operate during embryonic myogenesis and are re-activated in adult myogenesis. One such signalling pathway, Sonic hedgehog (Shh) signalling, controls several aspects of myogenesis in the embryo and previous studies have indicated that it plays a role in adult myogenesis. However, it remains unclear whether Shh signalling acts upon satellite cells or non-myogenic resident cells. This study builds on previous work in the lab showing that Shh signalling is cell-autonomously required in satellite cells for efficient muscle regeneration. Through a combination of ex vivo and in vivo genetic approaches, I demonstrated that up-regulation of Shh signalling increased the proliferation of satellite cells by accelerating their entry into cell cycle and progression through the cycle program. Up-regulation of Shh signalling in satellite cells altered also the balance between self-renewal and differentiation, by promoting asymmetric cell division at the expense of symmetric cell division. Given the involvement of Shh signalling in tumour development in other systems and in skeletal muscle tumours i.e. Rhabdomyosarcoma (RMS), the present study may provide novel insights into the role of Shh signalling in the pathogenesis of RMS through the deregulation of satellite cell homeostasis.
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7

Praski, Alzrigat Lisa. "Constraints on up-regulation of drug efflux in the evolution of ciprofloxacin resistance". Doctoral thesis, Uppsala universitet, Institutionen för medicinsk biokemi och mikrobiologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-320580.

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The crucial role of antibiotics in modern medicine, in curing infections and enabling advanced medical procedures, is being threatened by the increasing frequency of resistant bacteria. Better understanding of the forces selecting resistance mutations could help develop strategies to optimize the use of antibiotics and slow the spread of resistance. Resistance to ciprofloxacin, a clinically important antibiotic, almost always involves target mutations in DNA gyrase and Topoisomerase IV. Because ciprofloxacin is a substrate of the AcrAB-TolC efflux pump, mutations causing pump up-regulation are also common. Studying the role of efflux pump-regulatory mutations in the development of ciprofloxacin resistance, we found a strong bias against gene-inactivating mutations in marR and acrR in clinical isolates. MIC and fitness measurements revealed that amino acid substitutions conferred smaller susceptibility reductions and smaller fitness costs than gene-inactivating mutations, suggesting that resistance mutations in clinical isolates are selected for high fitness rather than high resistance (Paper I and II). We asked whether the high fitness costs of marR-inactivating mutations could be ameliorated without affecting the resistance phenotype. Multiple independent lineages were experimentally evolved to select for improved growth fitness. Whole genome sequencing revealed mutations affecting marA, lon and arcA as potential compensatory pathways. For the marA and lon mutations the improved growth rate was associated with an increased susceptibility (arcA is being investigated). (Paper III). An evolution experiment selecting for ciprofloxacin resistance revealed upon whole genome sequencing the expected mutations in drug target and efflux-regulatory genes, but also in genes encoding aminoacyl-tRNA synthetases. We investigated two independently selected leuS mutations, and concluded that they contributed to ciprofloxacin resistance by activating the stringent response that in turn caused up-regulation of genes involved in efflux. However, these leuS mutations incur a high fitness cost (Paper IV). To summarize, the research findings in this thesis suggest that the potential ciprofloxacin resistome may include more genes than previously thought, but a strong selection for high fitness selectively purifies many resistance mutations from clinical isolates. In conclusion, selection for high relative fitness constrains the spectrum of mutations that survive and get fixed in clinical populations of bacteria.
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8

McElroy, Anita K. "The mechanisms and consequences of cyclin E up-regulation in HCMV-infected cells /". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2000. http://wwwlib.umi.com/cr/ucsd/fullcit?p9988319.

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9

Woodford, Darryl Paul. "Regulating online : participant-driven approaches". Thesis, Queensland University of Technology, 2014. https://eprints.qut.edu.au/68800/1/Darryl%20Paul_Woodford_Thesis.pdf.

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This thesis considers and evaluates different approaches to regulating online gaming communities, including traditional top-down regulation, as well as bottom-up and hybrid forms led by participants. I examine the regulatory environment in both the video game and gambling industries through case studies of the science fiction, massively multiplayer game Eve Online and offshore gambling platforms and their community sites. I identify that the participant driven approach to regulation sometimes used in the offshore gambling industry was dependent on a number of factors, notably the strength of the community and the risks to platform operators of negative publicity. By subsequently comparing this to the video gaming industry, I suggest that participant driven processes may be an appropriate way to resolve disputes in the games industry, and show how these are – to a limited extent – already being applied.
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10

Lochmatter, Priska. "Cytokine selection and CD69 up-regulation in the diagnosis of delayed-type drug hypersensitivity". Bern : [s.n.], 2009. http://www.zb.unibe.ch/download/eldiss/09lochmatter_p.pdf.

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11

Closkey, R. M. C. "E6/E7 up-regulation of nucleophosmin is important for proliferation and inhibition of differentation". Thesis, Queen's University Belfast, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.517089.

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12

Hebbard, Lionel Warren [Verfasser]. "Up-regulation of casein-like proteins during rat pancreatic carcinoma progression / Lionel Warren Hebbard". Karlsruhe : KIT-Bibliothek, 1998. http://d-nb.info/1198222018/34.

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13

Matsuyama, Tomonori. "Midazolam inhibits the hypoxia-induced up-regulation of erythropoietin in the central nervous system". Kyoto University, 2015. http://hdl.handle.net/2433/202803.

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14

BOCCHETTA, Simone. "Up-regulation of the ATP-binding cassette transporter A1 inhibits hepatitis C virus infection". Doctoral thesis, Università del Piemonte Orientale, 2014. http://hdl.handle.net/11579/45964.

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15

Volokhov, Rachael N. "Does greater working memory predict greater skill in the up- and down-regulation of positive emotion?" Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1275654132.

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16

Armour, Danielle Louise. "Role of 11β-hydroxysteroid dehydrogenase type 2 in protection against inflammation during atherogenesis : studies in the Apoe-/- /11β-HSD2-/- double knockout mouse". Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/4431.

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It is well established that atherosclerosis, an inflammatory response to chronic injury in the blood vessel wall, plays a leading role in the development and progression of cardiovascular disease. Mineralocorticoid receptor (MR) over-activation has been implicated in atherosclerosis. In mineralocorticoid-target tissues, 11β- Hydroxysteroid dehydrogenase type 2 (11β-HSD2) inactivates glucocorticoids, conferring aldosterone specificity upon the normally unselective MR. Recent evidence suggests that 11β-HSD2 may also afford protection of MR in the cells of the vasculature, providing possible mechanisms by which MR activation may directly promote atherosclerosis. Consistent with this, Apoe-/-/11β-HSD2-/- double knockout (DKO) mice show accelerated atheroma development. The present thesis tested the hypothesis that inactivation of 11β-HSD2, allowing inappropriate activation of MR in cells of the vasculature, accelerates atherogenesis through promotion of a pro-inflammatory environment with increased endothelial cell expression of adhesion molecules and subsequent macrophage infiltration into plaques. DKO mice received either the MR antagonist eplerenone (200mg/kg/day) or vehicle in normal chow diet from 2 months of age for 12 weeks. Eplerenone significantly decreased atherosclerotic burden in brachiocephalic arteries of DKO mice, an effect that was accompanied by alterations in the cellular composition of plaques such that a more stable collagen- and smooth muscle cell- rich plaque was formed. Eplerenone treatment was also associated with a reduction in vascular inflammation as demonstrated by a significant reduction in macrophage infiltration into DKO plaques. The accelerated atherogenesis in DKO mice was clearly evident by 3 months of age, a time point at which Apoe-/- mice were completely lesion free. By 6 months, some Apoe-/- mice had developed lesions whilst all DKO mice at this age showed much larger plaques. Compared to Apoe-/- mice, the cellular composition of DKO plaques was altered favouring vulnerability and inflammation, with increased macrophage and lipid content and decreased collagen content. To investigate the possible underlying mechanisms responsible for increased inflammatory cell content, the expression of vascular cell adhesion molecule 1 (VCAM-1) was compared in DKO and Apoe-/- brachiocephalic arteries. VCAM-1 immunostaining was significantly greater on the endothelial cells of DKO arteries at 3 months compared to age-matched Apoe-/- mice. At 6 months, DKO and Apoe-/- mice had similar expression of VCAM-1. Finally, mouse aortic endothelial cells (MAECs) were used to investigate the mechanism of adhesion molecule up-regulation in the absence of 11β-HSD2. Both aldosterone and TNF-α, included as a positive control, dramatically increased VCAM-1 expression in MAECs. Spironolactone pre-treatment blocked the effect of aldosterone, suggesting an MR-mediated mechanism. Corticosterone alone had no effect on VCAM-1 expression. However, inhibition of 11β-HSD2 by pre-treatment with glycyrrhetinic acid allowed corticosterone to induce a significant increase in the number of VCAM-1-stained MAECs, demonstrating functional expression of 11β- HSD2 in MAECs. Consistent with 11β-HSD2 involvement, VCAM-1 up-regulation by corticosterone in the presence of glycyrrhetinic acid was reversed by blockade of MR with spironolactone. In conclusion, loss of 11β-HSD2 activity leading to inappropriate activation of MR in atherosclerotic mice promotes plaque vulnerability and increases vascular infiltration of macrophages which accelerates plaque growth, possibly through enhanced MR- mediated endothelial cell expression of VCAM-1.
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17

Larner, Stephen Frank. "Up-regulation and activation of caspase-12 and caspase-7 following traumatic brain injury in rats". [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0006609.

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Thesis (Ph.D.)--University of Florida, 2004.
Typescript. Title from title page of source document. Document formatted into pages; contains 139 pages. Includes Vita. Includes bibliographical references.
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18

Chen, Edwin. "Oxidative stress induces up-regulation of elongation factor-1 alpha (EF-1Ã) en route to apoptosis". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0033/MQ64330.pdf.

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19

Chen, Edwin 1975. "Oxidative stress induces up-regulation of elongation factor-1 alpha (EF-1ℓ) en route to apoptosis". Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=30354.

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During myocardial infarction, significant myocardial cell loss occurs in a process termed "post-ischemic reperfusion injury", a two-step process where the myocardium first undergoes temporary conditions of ischemia caused by an occlusion of blood flow, followed by the re-establishment of blood flow to the previously hypoxic myocardium. It is believed that the excessive production of reactive oxygen intermediates, such as free radicals and pro-oxidants, during the reperfusion process is a major contributing factor to the observed cell death. In the present study, we sought to investigate the role of the prooxidant, hydrogen peroxide (H2O2), in triggering apoptosis in H9c2(2-1) cells, a clonogenic cell line derived from embryonic rat heart ventricles. We demonstrate that there is a rapid up-regulation of elongation factor alpha1 alpha (EF-1alpha) en route to apoptosis initiated by an oxidative insult in vitro and in vivo, and that this phenomenon may be a necessary early event in the induction of apoptosis. (Abstract shortened by UMI.)
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20

Fan, Yan, Ping Chen, Ying Li, Gregory A. Ordway i Meng Yang Zhu. "Effects of Desipramine Treatment on Stress-Induced up-Regulation of Norepinephrine Transporter Expression in Rat Brains". Digital Commons @ East Tennessee State University, 2015. https://dc.etsu.edu/etsu-works/8597.

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Rationale Many studies demonstrate down-regulation of the norepinephrine transporter (NET) by desipramine (DMI) in vitro and in stress-naive rats. Little is known regarding regulation of the NET in stressed animals. Objective The present study was designed to investigate effects of DMI on the expression of NET and protein kinases in the stress rat. Methods Adult Fischer 344 rats were subjected to chronic social defeat (CSD) for 4 weeks. DMI (10 mg/kg, intraperitoneal (i.p.)) was administered concurrently with CSD or 1 or 2 weeks after cessation of CSD. Sucrose consumption, NET expression, and protein kinases were measured. Results CSD significantly increased messenger RNA (mRNA) and protein levels of NET in the locus coeruleus, as well as NET protein levels in the hippocampus, frontal cortex, and amygdala. These effects were nearly abolished when DMI was administered concurrently with CSD. CSD-induced upregulation of NET expression in the locus coeruleus, hippocampus, and amygdala lasted at least 2 weeks after cessation of CSD, an effect that was significantly attenuated by 1 or 2 weeks of DMI treatment starting from cessation of the CSD. Concurrent administration of DMI with CSD did not markedly interfere with CSD-induced decreases in protein levels of protein kinases A and C in these brain regions, but it did reverse the CSD-induced reduction in phosphorylated cAMP response element-binding (pCREB) protein levels in most brain regions. Conclusion These findings suggest that NET regulation by DMI occurs in both stressed and behaviorally naive rats, and DMI-induced changes in pCREB may be involved.
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21

Shipley, Lindsey C. BS, Harika MD Balagoni, Janet Lightner, Victoria PhD Palau i Koyamangalath MD Krishnan. "15 Lox 1 Up-regulation and Cytotoxicity with γ-tocotrienol in HCT-116 Colon Cancer Cells". Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/154.

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Colorectal cancer is the second leading cause of cancer-related deaths in the United States and the third most common cancer in men and women. Vitamin E is a lipid soluble antioxidant that exists as eight structurally different isoforms of tocopherols and tocotrienols. Recent experimental, and molecular studies suggest that γ-tocotrienol (GT3) may be a more potent cancer-preventive form of vitamin E. 15-lipoxygenase-1 (15-LOX-1) and its product 13-S-hydroxyoctadecadienoic acid (13-S-HODE) are decreased in colon cancer cells. 15 LOX-1 is considered a tumor suppressor gene in colon carcinogenesis. Non-steroidal anti-inflammatory drug (NSAID)-induced 15-LOX-1 expression is critical to aspirin and NSAID-induced apoptosis in colorectal cancer cells. HCT-116 is a microsatellite-instability (MSI) colon cancer cell line. MSI is a marker of chemo-resistance but is associated with improved survival as compared to microsatellite-stable (MSS) colon cancers. The effects of GT3 on cytotoxicity and 15 LOX-1 expression was studied on the human colon cancer cell line HCT-116. HCT-116 colon cancer cell lines were cultured in DMEM media and dosed with increasing concentrations of GT3 (20µM-50µM). Cytotoxicity of the drugs was studied using Cell Titer Glo and MTS assays 24 hours after dosing. Cells were then plated in 6-well plates and grown for 24 hours. Cells were then dosed with 2 mL of GT3 at 20 uM at the respective time periods (2h, 4h, 6h, 12h, 16h, 24h) and lysates were harvested. Gel electrophoresis was run according to BCA protein assay from the time-dependent lysates and blots were tagged with a rabbit 15-lox antibody. Ongoing experiments include RNA PCR. RNA is being isolated at 2, 4, 6 and 12 hours. The RNA as reversed transcribed using a 15 lox 1 primer and that cDNA is being quantified using Quantitative PCR. GT3 induced cytotoxicity in MTS assay and Cell Titer Glo assay when added to HCT-116 cell line. 15 LOX 1 protein expression was found to be up-regulated in the colon cancer cell line HCT-116 when GT3 was added at 12h, 16h and 24h with the maximum expression at 16 hours. Chemotherapeutic drugs can have significant side effects. Understanding the role of GT3 on colon cancer cell lines could lead to the development of novel drugs to supplement current chemotherapy regimens and allow for lower doses of chemotherapeutic agents. Modulation of 15-LOX-1 suggests that GT3 may induce apoptosis through induction of the lipoxygenase pathway. Further experiments are under way to study the mechanism of action of GT3 on the 15 LOX-1 pathway. Since HCT-116 is a MSI- colon cancer cell line, effects of GT3 on MSS- colon cancer cell lines will also be studied.
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Maeno, Atsushi. "Up-Regulation of miR-582-5p Regulates Cellular Proliferation of Prostate Cancer Cells Under Androgen-Deprived Conditions". Kyoto University, 2015. http://hdl.handle.net/2433/199165.

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23

Wilfong, Erin R. "The role of nerve growth factor in neuropeptide up-regulation in trigeminal ganglia neurons following irritant exposure". Morgantown, W. Va. : [West Virginia University Libraries], 2003. http://etd.wvu.edu/templates/showETD.cfm?recnum=3109.

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Thesis (Ph. D.)--West Virginia University, 2003.
Title from document title page. Document formatted into pages; contains xiii, 82, [148] p. : ill. (some col.). Includes abstract. Includes bibliographical references.
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24

PAL, KOUSTAV. "EXPLORING CHANGES IN HIGHER-ORDER GENOME ORGANISATION DURING THE COORDINATED TRANSCRIPTIONAL UP-REGULATION IN DROSOPHILA DOSAGE COMPENSATION". Doctoral thesis, Università degli Studi di Milano, 2019. http://hdl.handle.net/2434/609010.

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Dosage compensation (DC) is a highly plastic process responsible for altering transcriptional regulation, so as to preserve homeostasis in species with different karyotypes in the sexes. Over the past several decades this process has emerged as a robust model for understanding the relationship between transcriptional regulation and higher-order chromatin structure. In Drosophila melanogaster DC, the single male chromosome X undergoes an average two-fold transcriptional up- regulation for balancing the transcriptional output between sexes. Previous literature evidences proposed that a global change in chromosome structure may accompany this process. Recent studies in other model systems suggested that chromosome X in response to dosage compensation shows a highly altered structure. Namely, in mammals it loses all genome compartmentalisation post silencing by Xist, and in C. elegans it shows altered insulation post reduction of gene expression. All of these studies were based on Hi-C. Yet, in case of drosophila, no such structural changes were found using Hi-C. This raises questions regarding the sensitivity of Hi-C in cases where transcription un-regulation is localized, and questions the mounting evidence in literature showing a causal link between transcriptional processes and higher-order chromatin structure. Here I show that global conformational differences are indeed present in the male X chromosome and are detectable using Hi-C data on sex-sorted embryos alongside male and female cell lines. This task, was only made possible with the implementation of novel data analyses solutions. I show that the male X chromosome presents a more accessible structure. I identified differences in local genome compartmentalization, with several TAD boundaries disappearing or weakening in male X chromosome. These boundaries co-localize with features related to the binding of the dosage compensation complex. The strongest correlation we observed was in relation to a dosage compensation complex co-factor CLAMP, which shows differential binding pattern between the sexes. This protein was reported to enhance chromatin accessibility. I present conclusive evidence supporting a changing global chromosome structure in response to dosage compensation. I did not observe any differences in insulator binding. This in addition to change in insulation challenges the idea that insulation is a function of insulator binding. In the future, I would like to explore this avenue to understand how different players affecting genome functionality affect insulation as read-out from Hi-C data. In the course of this work, Hi-C data binned at higher resolutions tended to become extremely memory intensive. With this, I identified a need to develop a data handling solution which would allow me to work more efficiently with such high-resolution Hi- C datasets. Although, such solutions have been described for python, no such solution exists for R. I aimed to create an on-disk database which circumvents the problem of loading data into memory, solves its own dependencies and plays well with existing Hi-C formats. To address these aims, I developed HiCLegos, a package built for the R statistical environment. HiCLegos, implements an on-disk HDF data structure for storing and manipulating Hi-C data. HiCLegos is deployed as a Bioconductor package. This ensures better dependency solving and higher visibility from a growing community of biology focused developers. Finally, HiCLegos provides methods for loading 2D matrices and consortium generated sparse matrix files. From a user perspective, HiCLegos offers analysis centred methods for data retrieval, such as retrieving data for genomic loci separated by a certain distance.
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25

Schonberger, Robert Brian. "Upregulation of Hypoxia-Inducible Genes in Endothelial Cells to Create Artificial Vasculature". Yale University, 2006. http://ymtdl.med.yale.edu/theses/available/etd-06282006-142557/.

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This study explored the possibility that upregulation of Hypoxia Inducible Factor-1 (Hif-1)-responsive genes in Human Umbilical Vein Endothelial Cells (HUVEC) would promote and stabilize HUVEC formation into inchoate vascular beds within artificial collagen gels. This experiment was designed to explore the above possibility by sub-cloning Hif-1[alpha], the related chimeric construct Hif-1[alpha]/VP16, and the marker gene dsRed into retroviral expression vectors, producing retroviral vectors containing these genes, and stably transducing HUVEC using these retroviruses. Transduced HUVEC were to be observed in cell culture as well as after implantation into artificial collagen gels that have previously supported vascular bed formation by HUVEC. Our results show, preliminarily, that HUVEC transduced with Hif-1[alpha]/VP16 go into cell-cycle arrest. Attempts to transduce HUVEC with Hif-1[alpha] failed to achieve high enough transduction efficiency to determine the cells angiogenic potential. This study concluded that more experiments need to be conducted to better characterize the effects of hypoxia-responsive gene upregulation in controlling HUVEC angiogenesis and cell-cycle signaling and that straightforward transduction of HUVEC by Hif-1[alpha]/VP16 is probably not sufficient, in itself, to induce in vitro vascular bed formation.
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26

Zheng, Feihui, i 郑斐晖. "Up-regulation of alpha-enolase (ENO1) by HIF-1α in retinal pigment epithelial cells after hypoxic challenge is not involved in the regulation of VEGF secretion". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/208585.

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Choroidal neovascularization (CNV) is a leading threat to severe vision loss, particularly in patients with age-related macular degeneration (AMD). In CNV, newly formed blood vessels sprout from the choroid to the sub-retinal space, where leakage and bleeding of the abnormal vessels lead to photoreceptor death and subsequent vision loss. It is believed that CNV is mediated by growth factors (e.g. vascular endothelial growth factor {VEGF}) produced by the retinal pigment epithelium (RPE) under pathological states (e.g. hypoxia). Current treatments for CNV aiming at countering VEGF only help decrease leakage and inhibit formation of CNV, but none of them is curative and the recurrence rate remains high. In order to find other more powerful potential therapeutic targets, the regulations of VEGF signaling in the pathophysiology of CNV is the focus of numerous translational investigations. Previously, Hypoxia-inducible factor-1 (HIF-1), a crucial transcriptional factor in response to hypoxia, is identified as the master transcriptional factor controlling VEGF expression in the RPE promoting CNV. Alpha-enolase (ENO1), a key glycolytic enzyme, is known to be over expressed in several types of carcinomas also under the regulation of HIF-1. ENO1 has been reported to be closely associated with cancer progression, angiogenesis, and venous invasion. The molecular events of ENO1 in the pathogenesis of promoting angiogenesis are of interest but still barely understood. Recently, the association of ENO1 antibodies with retina has been seen in patients with AMD. We hypothesize that ENO1 expression in the RPE may play a role in the development of CNV, participating in the regulation of VEGF. Hypoxia is an important pathological condition in the formation of CNV. Here, we first determined ENO1 expression and cell death in a human RPE cell line, ARPE-19, under cobalt (II) chloride (CoCl2)-induced hypoxia or anoxia (95% N2, 5% CO2). To further investigate the regulation of ENO1 in CNV, HIF-1α-diminished RPE cells were generated using small interfering RNA (siRNA) and the change of ENO1 expression in response to hypoxic injury was determined. Upon 24 hr of treatment with CoCl2-induced hypoxia or anoxia, the expression of ENO1 and VEGF increased significantly along with HIF-1α in ARPE-19 cells, both of which could in turn be significantly down-regulated by HIF-1α siRNA. Interestingly, cell death remained low in ARPE-19 cells, even after 24 hr of CoCl2-induced hypoxia or anoxia. To further study the role of ENO1 in CNV, we started by investigating the relationship between ENO1 and VEGF. SiRNA was used to knock down the expression of ENO1 in ARPE-19 cells. Upon transfection with the siRNA, ENO1 expression was successfully down-regulated when treated with CoCl2-induced hypoxia. However, VEGF secretions from the ENO1-diminished ARPE-19 cells under CoCl2-induced hypoxia remained unchanged. Double knockdown of ENO1 together with HIF-1α by siRNA also did not help to further suppress VEGF secretion in the hypoxic ARPE-19 cells. Hence, ENO1 was demonstrated to be activated and up-regulated by HIF-1 in RPE cells responding to hypoxia, suggesting a potential role of ENO1 in favoring the formation of CNV, but not through influencing VEGF secretion.
published_or_final_version
Ophthalmology
Master
Master of Philosophy
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27

Li, Xiao Yu 1973. "Beta-adrenoreceptor mediated atria specific up-regulation of regulator of G-protein signaling (RGS) 5 in rodent atrium". Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=80318.

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Due to a 195 fold cardiac overexpression of beta2-Adrenoreceptor (beta2AR), the hearts of transgenic TG4 mice are chronically overstimulated and, indeed, show little stimulatory response to further betaAR agonists. Previous investigations had suggested that signaling from the overexpressed beta 2ARs was dampened in the atria of TG4 mice. Regulators of G-protein Signaling (RGSs) are a family of negative regulators of G-Protein Coupled Receptor (GPCR) signaling that are frequently induced by GPCR stimulation. Using an RT-PCR based strategy, we have identified RGS5 as being a candidate RGS that is up-regulated in the atria of TG4 mice. Northern blot analysis demonstrated that RGS5 levels are 2--3 fold higher in the atria of TG4 mice when compared to their non-transgenic littermates. To further characterize RGS5 expression, we generated an RGS5 specific anti-serum. Results indicate that RGS5 is a housekeeping RGS in the heart and in skeletal muscle but its betaAR mediated induction in the atria suggests that it also has a highly specialized function.
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28

ACQUARONE, ERICA. "Synaptic and Memory Dysfunction Induced by Tau Oligomers is Rescued by Up-regulation of the Nitric Oxide Cascade". Doctoral thesis, Università degli studi di Genova, 2019. http://hdl.handle.net/11567/942799.

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Background: Soluble aggregates of oligomeric forms of tau protein (oTau) have been associated with impairment of synaptic plasticity and memory, therefore representing a critical hallmark in the etiopathogenesis of Alzheimer’s disease. However, the molecular mechanisms underlying the Synaptic and memory dysfunction induced by elevation of oTau are still unknown. Methods: Using a combination of biochemical, electrophysiological and behavioral techniques, phosphorylation of the cAMP-responsive element binding (CREB) protein, a transcriptional factor involved in memory, as well as long-term potentiation (LTP), a type of synaptic plasticity thought to underlie memory formation, and both short-term spatial and associative memory, were examined following oTau elevation with/out up-regulating the nitric oxide (NO) cascade. Results: Phospho-CREB increase occurring during memory formation was found to be reduced after oTau elevation during memory formation. This lead us to explore whether upregulation of various components of the NO signaling pathway impinging onto CREB is capable of rescuing oTau-induced impairment of synaptic plasticity, memory and CREB phosphorylation. Increased NO levels protected against oTau-induced impairment of LTP. This beneficial effect involved the activation of soluble guanylyl cyclase and elevation of cGMP levels, which stimulate cGMP-dependent protein kinases (PKG). Pharmacological inhibition of cGMP degradation through inhibition of phosphodiesterase 5 rescued oTau-induced LTP reduction. Activation of PKG rescued oTau-induced LTP and memory impairments. Finally, elevation of cGMP levels re-established normal CREB phosphorylation after LTP induction in the presence of oTau. Conclusions: Up-regulation of CREB activation through agents acting on the NO cascade might be beneficial against tau-induced synaptic and memory dysfunctions
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29

King, R. Glenn. "On the immunological roles of TLT2 and HSH2". Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2008r/king.pdf.

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30

Koops, Marten Derek. "Transcriptional regulation of human nonspecific cross-reacting antigen, a carcinoembryonic antigen gene family member up-regulated in colorectal carcinomas". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0005/MQ44198.pdf.

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31

Koops, Marten Derek. "Transcriptional regulation of human nonspecific cross-reacting antigen, a carcinoembryonic antigen gene family member up-regulated in colorectal carcinomas". Thesis, McGill University, 1997. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=20829.

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Human nonspecific cross-reacting antigen (NCA), a close relative of the tumour marker human carcinoembryonic antigen (CEA), is also an in vitro homotypic intercellular adhesion molecule capable of inhibiting differentiation when expressed ectopically in myoblasts. Moreover, NCA appears to be overexpressed at the transcriptional level to a greater extent and more frequently in colorectal carcinomas than CEA. This study examines the transcriptional control mechanisms responsible for orchestrating NCA expression. The region within 283 bp upstream of the translational start site of the NCA gene was found to be capable of directing high levels of expression in functional promoter assays. Footprinting experiments identified three cis-acting elements and mobility-shift assays revealed that the first of these elements is bound by USF1 and USF2, and the second two are bound by Sp1 and Sp3. No cis-acting elements corresponding to CEA FP4 or the silencer CEA FP5 of the CEA promoter were detected in the NCA promoter, which may contribute to the differential expression of NCA versus CEA in tumourigenesis.
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32

Schütte, Verena [Verfasser]. "The Mannose receptor induces T cell tolerance via inhibition of CD45 and up‐regulation of CTLA-4 / Verena Schütte". Bonn : Universitäts- und Landesbibliothek Bonn, 2014. http://d-nb.info/1077289448/34.

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33

Isobe, Ken-ichi, Masashi Akiyama, Sachiko Ito, Naomi Nishio i Mayu Hara. "Up-regulation of Gr1^+CD11b^+ cell population in the spleen of NaClO-administered mice works to repair skin wounds". Thesis, Biodiscovery, 2012. http://hdl.handle.net/2237/18821.

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34

Cashman, Adrian Christopher. "Topping up or watering down? : can regulation support sustainability? : the case of the water industry of England and Wales". Thesis, University of Sheffield, 2004. http://etheses.whiterose.ac.uk/12843/.

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Water is the most invisible of the visible means of existence in our post-modern society. It is a defining characteristic that unites our natural, social and economic world and is fundamental for life and health. However, given its multiple characteristics the management of water is a complex and often contradictory task that has led to an on-going quest for acceptable solutions. As if this were not problem enough, the last few decades have seen concepts of sustainability become overtly important principles, impacting on the governance of the water sector. A consequence of this rise in importance of sustainability to society, business and the state has been the enclosure and accommodation of sustainability within modes of governance, regulation and accountability. Instead of treating sustainability, regulation and accountability as separate centres of enquiry, this work treats them as a complex set of interrelated systems that both respond to and produce change. The work therefore draws on a variety of theoretical perspectives that together broadly outline the contours of the political economy of water management. The theoretical framework has been used to provide an interpretation of the data gathered from fieldwork interviews from across the water sector and documentary sources. In doing so, the inquiry has focused on a particular period of time, 1997-2001, in order to illuminate the processes and forces at work in the evolution of modes of regulation with respect to sustainability. The inquiry indicates the multi-level nature of the development of governance and regulatory processes, firmly rooted within a weak sustainability paradigm. It is argued that how sustainability issues are resolved depends upon institutional structures. For progress towards a more sustainable future civil society must be re-embedded in economic activities in order to bring about change in cognitive knowledge, values and norms.
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35

Yamanaka, Kenya. "Olprinone Attenuates Excessive Shear Stress Through Up-Regulation of Endothelial Nitric Oxide Synthase in a Rat Excessive Hepatectomy Model". Kyoto University, 2012. http://hdl.handle.net/2433/157435.

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36

Saab, Tara K. "Pollution from septic systems, assessing the implementation of Ontario EPA Regulation 358 and the Clean Up Rural Beaches (CURB) program". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ39875.pdf.

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37

Chang, Yueming. "Investigation of two early events in amyotrophic lateral sclerosis mRNA oxidation and up-regulation of a novel protective factor MSUR1 /". Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1196182155.

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38

Yamauchi, Ryoko. "Up-regulation of SR-PSOX/CXCL16 and recruitment of CD8[+] T cells in cardiac valves during inflammatory valvular heart disease". Kyoto University, 2004. http://hdl.handle.net/2433/147487.

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39

Johnson, Hope N. "From the ground up: An analysis of the international regulation of agriculture using a rights-based approach to food security". Thesis, Queensland University of Technology, 2016. https://eprints.qut.edu.au/99631/6/Hope_Johnson_Thesis.pdf.

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This project is the first time the international laws regulating agriculture have been systematically identified and collectively critically analysed. One of the biggest challenges facing humanity is how to ensure food security in changing climatic conditions with growing natural resource scarcity and an increasing population. The role of law and policy in this context is to influence actions and shape outcomes. Accordingly, the thesis developed a conceptual basis for evaluating the many and varied international legal and policy instruments drawing on human rights, security and environmental principles. Using this as the benchmark, the research explored the gaps, overlaps and inconsistencies in the international regulatory framework for agriculture and formulated reform recommendations for a food secure future.
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40

VERGINELLI, FEDERICA. "Notch signaling involvement in endothelial responses to inflammation: Jagged1 and Notch1 mediate IL-1b iInduced up-regulation of adhesion molecules". Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2010. http://hdl.handle.net/2108/1250.

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Obiettivo--Il signaling di Notch, attraverso l’attivazione dei recettori Notch1 e Notch4, gioca un ruolo chiave nella determinazione e nell’omeostasi dell’endotelio. Il TNFa determina la down-regolazione di Notch4 e del target gene Hes1, e questa modulazione causa la perdita della quiescenza e l’induzione della molecola di adesione vasale (VCAM-1) nelle cellule endoteliali (ECs). Questo studio mira ad investigare la regolazione dei componenti del signaling di Notch indotta dall’IL-1b ed il loro coinvolgimento nell’up-regolazione delle molecole di adesione. Metodi e Risultati--Abbiamo dimostrato che l’IL-1b induce una forte up-regolazione di Jagged1, e mentre l’attivazione di Notch4 diminuisce, la forma attiva di Notch1 (Notch1ICD) rimane costante. La complessiva inibizione del signaling di Notch, attraverso un inibitore della g-secretasi, determina una riduzione nell’up-regolazione di VCAM-1 indotta dall’IL-1b. Inoltre, il silenziamento di Jagged1 ha un effetto negativo sull’up-regolazione delle molecole di adesione indotta dall’IL-1b e il doppio silenziamento di Jagged1 e Notch1 determina un effetto ancora maggiore. In aggiunta, la forzata over-espressione di Notch1ICD induce l’espressione di VCAM-1, e questo effetto aumenta dopo il trattamento con l’IL-1b. Nelle cellule over-esprimenti Notch1ICD, inibendo chimicamente la traslocazione nucleare di NF-kB indotta dall’IL-1b, non si riduce significativamente l’up-regolazione di VCAM-1. In fine, l’over-espressione di Hes1, durante il trattamento con l’IL-1b, inibisce l’up-regolazione delle molecole di adesione e reprime la trascrizione di Jagged1, indicando un loop regolativo negativo tra i componenti del signaling di Notch. Conclusioni—Complessivamente i risultati indicano che Jagged1 segnala attraverso Notch1, e Notch1 e’ il recettore piu’ importante nella risposta infiammatoria delle ECs. Inoltre, in presenza di Notch1 l’induzione delle molecole di adesione risulta solo parzialmente dipendente da NF-kB.
Objective--Notch signaling plays a key role in endothelial determination and homeostasis through Notch 1 and Notch 4 receptors. In endothelial cells (ECs) the TNFa determines the down-regulation of Notch4 and Hes1 and this modulation are associated with the loss of quiescence and the up-regulation of vascular cell adhesion molecules-1 (VCAM-1), This study investigated the regulation of Notch signaling components upon IL-1β induction and their implication in the up-regulation of adhesion molecules. Methods and Results-- We showed that IL-1β induced a strong up-regulation of the Notch ligand Jagged1. Strikingly, while Notch4 activation decreased, Notch1 active form (Notch1ICD) remained constant. The global inhibition of Notch activation through a g-secretase inhibitor resulted in reduction of IL-1β-induced VCAM-1 up-regulation. Moreover, the silencing of Jagged1 partially affected the up-regulation of adhesion molecules induced by IL-1b, and the double silencing of Jagged1 and Notch1 led to a higher reduction of the adhesion molecules expression after IL-1β treatment. Interestingly, Notch1ICD forced expression induced VCAM-1 expression in ECs and increased the up-regulation induced by IL-1β treatment. Chemical inhibition of the NF-kB nuclear translocation induced by IL-1β treatment did not significantly reduce VCAM-1 expression in Notch1ICD expressing cells. Finally, Hes1 over-expression during IL-1β treatment inhibited the up-regulation of adhesion molecules and, concomitantly, repressed Jagged1 trascription, suggesting a negative regulative loop between Notch signaling component. Conclusions--All together our results indicate that, Jagged1 sustains Notch1 activation that specifies the effects of IL-1β. Thus, Notch1 is the most important receptor involved in inflammatory responses of ECs, and its function is, at least in part, NF-kB-dependent.
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41

Dromey, Jasmin Rachel. "Elucidating novel aspects of hypothalamic releasing hormone receptor regulation". University of Western Australia. School of Medicine and Pharmacology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0133.

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[Truncated abstract] G-protein coupled receptors (GPCRs) form one of the largest superfamilies of cell-surface receptors and respond to a vast range of stimuli including light, hormones and neurotransmitters. Although structurally similar, GPCRs are regulated by many diverse proteins, which allow the specific functions of each receptor to be carried out. This thesis focussed on two well-documented GPCRs, the thyrotropin releasing hormone receptor (TRHR) and gonadotrophin-releasing hormone receptor (GnRHR), which control the thyroid and reproductive endocrine pathways respectively. Although each of these anterior pituitary receptors is responsible for distinct physiological responses, both are integral to normal development and homeostasis. This thesis focused on three areas of GPCR regulation: ?-arrestin recruitment, transcription factor regulation and receptor up-regulation. The role of the cytoplasmic protein, ?-arrestin, has perhaps been previously underestimated in GPCR regulation, but it is now increasingly apparent that ?-arrestins not only inhibit further G-protein activation and assist in GPCR internalisation but also act as complex scaffolding platforms to mediate and amplify downstream signalling networks for hours after initial GPCR activation. It is therefore becoming increasingly important to be able to monitor such complexes in live cells over longer time-frames. ... Members of the E2F transcription family have been previously identified by this laboratory as potential GnRHR interacting proteins, via a yeast-2-hybrid screen and BRET. This thesis further investigated the role of E2F family members and demonstrates that a range of GPCRs are able to activate E2F transcriptional activity when stimulated by agonist. However, despite GnRHR displaying robust E2F transcriptional activation upon agonist stimulation, this did not result in any conclusive evidence for functional regulation, although it is possible E2F may modulate and assist in GnRHR trafficking. Furthermore it is apparent that E2F family members are highly redundant, as small effects in GnRHR binding and cell growth were only observed when protein levels of both E2F4 and E2F5 were altered. During the course of the investigation into the effect of E2F transcription on GPCR function, it was evident that long-term agonist stimulation of GnRHR had a profound effect on its expression. As this was explored further, it became clear that this agonist-induced up-regulation was both dose- and time-dependent. Furthermore, altering levels of intracellular calcium and receptor recycling/synthesis could modulate GnRHR up-regulation. In addition, an extremely sensitive CCD camera has been used for the first time to visualise the luciferase activity attributed to GnRHR up-regulation. Overall, this thesis demonstrates the complex nature of GPCR regulation. For the first time, long-term BRET analysis on ?-arrestin interactions with both classes of GPCRs has been examined in a variety of cellular formats. This has given valuable insights into the roles of phosphorylation and internalisation on ?-arrestin interaction. Additionally, this thesis has revealed that prolonged agonist exposure increases receptor expression levels, which has major implications for drug therapy regimes in the treatment of endocrine-related disorders and tumours.
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42

Li, Ling. "Mechanisms Underlying Apoptosis Inhibition and Transcription Repression by Ski". Connect to text online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1118235807.

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43

Bastien, Jérémie. "Le football professionnel européen dans un système capitaliste financiarisé en crise : une approche régulationniste des facteurs de changement institutionnel". Thesis, Reims, 2017. http://www.theses.fr/2017REIME002/document.

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L’idée que le football professionnel en Europe est en crise fait très largement consensus parmi les économistes. Dans notre thèse, nous montrons que ce diagnostic suppose de négliger un certain nombre d’éléments constitutifs de l’inscription du football dans le monde économique. C’est pourquoi, nous défendons que, loin d’être en crise, le football professionnel européen est, depuis les années 1980, dans une phase de très forte croissance. Pour ce faire, nous adoptons une démarche mésoéconomique régulationniste et procédons à une analyse systémique et multi-niveaux du football professionnel européen. Nous aboutissons ainsi à la caractérisation d’un « régime économique de fonctionnement » que nous qualifions de « financiarisé » compte tenu de l’instrumentalisation du football par des intérêts financiarisés et de leur influence sur les stratégies des acteurs traditionnels du football. Cette financiarisation du football engendre une forte instabilité de son régime puisque l’activité des clubs implique du déficit et du surendettement. En effet, l’incitation à la performance sportive (ligue ouverte), le fort pouvoir de négociation des joueurs (hold-up) et la souplesse de l’environnement réglementaire du football conduisent les clubs à des niveaux de dépenses élevés. Au contraire des « petits » clubs, cette situation n’est pas problématique pour les « grands » clubs, puisqu’ils sont soutenus par des agents à forte capacité de financement et tirent des revenus élevés de leur participation aux compétitions supranationales. Dans ce contexte, le régime est donc durable : sous l’effet de l’instabilité, les acteurs nouent de nouveaux compromis qui modifient les « dispositifs institutionnels » existants et rendent ainsi pérenne la logique de croissance en vigueur. Il y a donc régulation (au sens de la théorie de la régulation) du football. Il reste toutefois que ces modalités de régulation conduisent à accroître les inégalités entre les clubs et que cela pourrait, à terme, amener à une crise économique majeure du football professionnel européen
Economists argue that the European professional football is in crisis. This thesis discusses this postulate by testing the relationship between the changes in football and the transformations of modern capitalism. Our methodology is based on a meso-level analysis from the French “Régulation theory” which provides a systemic and multilevel analysis. The thesis thus emphasizes how the progressive integration of financialised interests in football has an influence on the strategies of football traditional stakeholders. It actually shows that the financialisation process of the European professional football leads to growth since the 1980s. However, this growth is rather unstable because losses and indebtedness are part of clubs activity. The incentive for sports performance (open league), the players’ strong bargaining power (hold-up) and the flexibility of the regulatory environment are the main determinants of the clubs’ high spendings. Contrary to the “small” clubs, this situation is not a constraint for the “big” clubs thanks to the financial contributions they obtain from their owners, from their funding partners and from their participation to supranational competitions. In this environment and despite instability, the growth regime remains nevertheless sustainable. The stakeholders create new compromises to reduce imbalances: these compromises are the roots for new institutional arrangements that finally support the growth logic which is in place. There is therefore a “régulation” in European professional football, that is to say a process that contributes to the reproduction of the sector. However, this process paradoxically increases inequalities and may encourage the conditions for a major economic crisis
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Yin, Yinfei. "Helicobacter pylori mediated hypergastrinaemia stimulates heparin-binding epidermal growth factor-like growth factor shedding via up-regulation of matrix metalloproteinase-7". Thesis, University of Nottingham, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491023.

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Gastric cancer is the second leading cause of cancer death worldwide. The strongest risk factor in the development of distal gastric cancer is Helicobacter Pylori (H. pylori) infection. Though the exact mechanism through which H. pylori contributes to gastric cancer progression is not yet fully elucidated, it may involve the downstream pathways triggered by hypergastrinaemia, which include induction of matrix metalloproteinases (mmps), and enhanced expression of growth factors.
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45

Kraft, Juliane Viktoria [Verfasser], i Sabine [Akademischer Betreuer] Windhorst. "Up-regulation of Biglycan is associated with poor prognosis and PTEN deletionin patients with prostate cancer / Juliane Viktoria Kraft ; Betreuer: Sabine Windhorst". Hamburg : Staats- und Universitätsbibliothek Hamburg, 2019. http://d-nb.info/1181328918/34.

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46

Fukui, Toshiro. "Gastric mucosal hyperplasia via up-regulation of gastrin induced by persistent activation of gastric innate immunity in MHC class 2-deficient mice". Kyoto University, 2006. http://hdl.handle.net/2433/143866.

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47

Aguilar, Fenollosa Ernestina. "Efecto de la gestión de la cubierta vegetal en el control biológico de Tetranychus urticae en mandarino clementino". Doctoral thesis, Universitat Jaume I, 2011. http://hdl.handle.net/10803/22694.

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Tetranychus urticae es una especie plaga importante en cítricos que puede también alimentarse de otras especies asociadas a la cubierta vegetal de este cultivo. Para determinar el efecto de la gestión de la cubierta vegetal en el control biológico de este ácaro, hemos estudiado la dinámica tanto de ácaros Tetranychidae como Phytoseiidae en cuatro parcelas comerciales de mandarino clementino en las que se aplicó tres estrategias diferentes de gestión de la cubierta vegetal: (1) suelo desnudo, (2) cubierta espontánea y (3) cubierta sembrada de Festuca arundinacea. Los resultados apuntan a que tanto los enemigos naturales (mecanismos "top-down") como la planta huésped (mecanismos "bottom-up") juegan un papel importante en la regulación de los ácaros Tetranychidae.

Por un lado, la selección de dos razas de T. urticae especializadas en F. arundinacea y en Citrus clementina, en la cubierta y en el árbol respectivamente, cuando esta gramínea se utiliza como cubierta podría explicar en parte los resultados obtenidos (regulación "bottom-up") ya que esto impediría a los especímenes de una planta huésped colonizar con éxito la otra. Los ensayos de trasplante recíproco realizados muestran que las dos demos de T. urticae recogidas de clementina y F. arundinacea difieren considerablemente en su éxito en el desarrollo en el huésped alternativo y esto indica la existencia de fenómenos de adaptación local.

Esta adaptación se traduciría en mecanismos "bottom-up" que evitarían que los ácaros que habitan en la cubierta colonicen con éxito la copa de los árboles.

Por otro lado, la composición cualitativa de las comunidades de Phytoseiidae asociados a las diferentes cubiertas podría ser clave en la regulación de las poblaciones de T. urticae y Panonychus citri (regulación "top-down"). Los ácaros Phytoseiidae tipo I y II, depredadores especializados en Tetranychidae, se encuentran de manera consistente en la cubierta de F. arundinacea y esto puede explicar la mejor regulación de las poblaciones de ácaros Tetranychidae en los árboles asociados a esta cubierta. Por el contrario, la disposición más regular de fuentes de alimentación alternativas (polen) en la cubierta natural en relación con la cubierta de F. arundinacea, podría explicar la mayor abundancia de Phytoseiidae tipo IV en la primera. Como consecuencia, los Phytoseiidae tipo I y II, más eficaces en el control de Tetranychidae, podrían sufrir las consecuencias de ser competitivamente inferiores que el Phytoseiidae generalista tipo IV que explota el polen en la cubierta espontánea. Este hecho, en combinación con los períodos de escasez de presa, podría dar lugar a su desaparición del agroecosistema y resultar en un deficiente control de los ácaros Tetranychidae en los árboles asociados a una cubierta natural.
Haciendo balance de gastos e ingresos, la cubierta más favorable fue la de F. arundinacea (entre 44,4 y 74,5% de reducción de costes en relación con la más cara). Festuca arundinacea como cubierta vegetal es una estrategia de control biológico por conservación muy recomendable para los productores de clementina. Aunque su uso no redujo las poblaciones de ácaros en los árboles por debajo del umbral económico, la disminución en la necesidad de tratamientos, hace que la adopción de esta táctica sea una alternativa beneficiosa tanto ecológica como económicamente.

Nuestros resultados apuntan a la cubierta de F. arundinacea, que no permitió el establecimiento de Tetranychus evansi y ofrece una mejor regulación de P. citri y T. urticae que en suelo desnudo o cubierta natural, como la más adecuada para un control más sostenible de los ácaros Tetranychidae en cítricos.

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48

Domingues, Rita B. "Bottom-up regulation of phytoplankton in the Guadiana estuary". Doctoral thesis, 2010. http://hdl.handle.net/10400.1/1558.

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Tese dout., Ciências do Mar (Ecologia Marinha), Faculdade de Ciências e Tecnologia, Univ. do Algarve, 2010
Phytoplankton are key players in the aquatic environment and they can be effectively used to understand and predict the functioning and production of aquatic ecosystems. Given that phytoplankton is affected by natural and human-induced perturbations, such as eutrophication and global climate change, it is pressing to understand which factors regulate phytoplankton communities. The main goal of this work was, therefore, to understand how phytoplankton growth and production in the turbid Guadiana estuary, particularly in the freshwater tidal zone, is regulated by bottom-up factors, namely nutrients and light. Enrichment bioassays were carried out to evaluate nutrient and light limitation of phytoplankton growth. Nutrient limitation, specifically by nitrogen, was observed during the productive period. Nitrogen, as nitrate, became limiting to phytoplankton growth at concentrations lower than 20 WM. Although nitrate was the main nitrogen source in the Guadiana estuary, an overall preference for ammonium was observed, mainly by cyanobacteria and green algae. Diatoms were the most nutrient-limited group, and they clearly preferred nitrate as their N-source. Regarding light availability, phytoplankton was not acclimated to the low light conditions that prevail in the Guadiana estuary and light limitation occurred throughout the year. Diatoms were the most light-limited group, whilst cyanobacteria seemed to be more acclimated to low light. Primary production was higher in the more turbid regions, where light availability was the lowest, but nutrient concentrations, although occasionally limiting, were the highest. Therefore, phytoplankton in such turbid regions were the most efficient in using limiting resources. River flow was a major regulator of nutrient and suspended matter inputs to the estuarine zone. Tidallyinduced variability of phytoplankton and environmental drivers in the freshwater tidal estuarine zone was low and resulted from seasonal and fortnightly variability in river flow and tidal currents.
Fundação para Ciência e Tecnologia (FCT) - 27536/2006)
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49

Shan, Shannon J. C. "Up-regulation of human tissue kallikrein 6 in ovarian cancer". 2006. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=450528&T=F.

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50

"Inflammation-induced up-regulation of hepcidin expression in the brain". 2013. http://library.cuhk.edu.hk/record=b5549291.

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鐵調素，作為關鍵的鐵調節激素，在維持外周系統的鐵平衡中具有重要作用。外周鐵調素的表達受到多種因素的平衡調節，包括鐵的狀態，炎症，造血活動和缺氧。這一激素肽在腦內的存在和廣泛分佈，提示它可能在腦鐵平衡中也發揮作用。本研究檢測了炎症是否對腦內鐵調素表達起調節作用，從而影響腦鐵代謝。
在本研究的第一部分，我們檢測了炎症是否調節腦內鐵調素的表達，以及這種調節作用在腦內是否具有區域特異性。利用脂多糖（一種廣泛使用的炎症誘導劑）誘導的炎症模型，我們發現腦室內注射脂多糖可區域特異性地誘導腦內鐵調素的表達，即誘導皮層和黑質的鐵調素表達，而海馬的鐵調素水準無顯著改變。與此相伴隨的是腦內膜鐵轉運蛋白區域特異性的表達下降。此外，我們發現脂多糖處理引起的腦內鐵調素表達升高發生在神經元而不是星形膠質細胞內。這些發現提示，炎症能夠區域特異性地上調腦內鐵調素表達，上調的鐵調素轉而下調特定腦區膜鐵轉運蛋白的表達。
在本研究的第二部分，我們檢測了離體水準上炎症對原代皮層神經元和MES23.5多巴胺能細胞鐵調素表達的影響。我們觀察了炎症對這些細胞鐵調素和膜鐵轉運蛋白表達的作用。我們發現脂多糖不增加原代皮層神經元鐵調素的表達。但在與BV-2小膠質細胞共培養的條件下，原代皮層神經元的鐵調素表達水準經脂多糖刺激後上升。我們檢測了一系列可能由小膠質釋放的促炎細胞因數對神經元鐵調素表達的影響。結果表明，白介素-6介導了脂多糖誘導的神經元鐵調素表達升高的作用。我們進一步發現，白介素-6在短時間內直接增加神經元鐵調素表達和降低膜鐵轉運蛋白表達。最後我們進一步探究了白介素-6對腦內鐵調素表達的調控機制，發現在原代皮層神經元和MES23.5多巴胺能細胞中白介素-6誘導的鐵調素表達是通過信號轉導和轉錄啟動因數3信號通路介導的。
綜上所述，我們的研究結果表明，炎症在調節腦內鐵調素表達和控制腦內鐵轉運中發揮重要的作用。在腦內，炎症區域特異性地誘導鐵調素表達上調和膜鐵轉運蛋白表達下調。白介素-6/ 信號轉導和轉錄啟動因數3這一信號通路介導了在炎症情況下腦內鐵調素表達。這些發現加強了我們對於腦內鐵調素表達的調節過程的理解，並提供了一種新的關於鐵調素在腦內抗炎作用的治療觀點。
Hepcidin, as the central iron regulatory hormone, plays a key role in maintaining peripheral iron homeostasis. The expression of hepcidin in the periphery is regulated by multiple factors homeostatically, including iron status, inflammation, erythropoietic activity and hypoxia. The presence and widespread distribution of this peptide in the brain suggests that hepcidin may also have an essential role in brain iron homeostasis. In this study we tested the hypothesis that inflammation exerts an important role in the regulation of brain hepcidin expression, which might alter brain iron metabolism.
To investigate whether inflammation could regulate brain hepcidin expression and whether this regulatory role is regionally specific in the brain, in the first part of study, we explored the effects of lipopolysaccharides (LPS), a widely used inflammation-inducing agent, on hepcidin expression in different brain regions of the rat brain in vivo. We found that intracerebroventricular (i.c.v.) injection of LPS induced brain hepcidin expression regionally specifically, that is, in the cortex and substantia nigra but not in the hippocampus. This effect was accompanied by a regionally specific decrease in brain ferroportin expression. Besides, brain hepcidin was found to be increased in neurons but not in astrocytes by LPS treatment. These findings indicate that inflammation could up-regulate brain hepcidin expression regionally specifically in the brain, which in turn down-regulates ferroportin expression in specific brain regions.
In the second part, we investigated the effects of inflammation on hepcidin expression in primary cortical neurons and MES23.5 dopaminergic cells in vitro. The expression of hepcidin as well as ferroportin was observed. We found that LPS did not increase hepcidin expression in primary cortical neurons. However, LPS induced neuronal hepcidin expression with the presence of BV-2 microglia cells. We examined the effects of a series of pro-inflammatory cytokines which could be released by microglia cells, on hepcidin expression, and found that interleukin-6 (IL-6) mediated neuronal hepcidin expression induced by LPS. Furthermore, we found that IL-6 directly increased hepcidin expression and decreased ferroportin expression in an acute manner. Finally, we further investigated the mechanisms underlying the regulatory effects of IL-6 on brain hepcidin expression, and found that IL-6-induced hepcidin expression is via signal transducer and activator of transcription-3 (STAT3) signaling in primary cortical neurons and MES23.5 dopaminergic cells.
In conclusion, the results of the present study implied that inflammation plays an important role in regulating brain hepcidin expression and controlling brain iron transport. In the brain, hepcidin up-regulation and ferroportin down-regulation is induced by inflammation in a regionally specific way. IL-6/ STAT3 signaling pathway is essential for brain hepcidin expression during inflammation. These findings enhance our understanding of the regulatory process of hepcidin in the brain, and provide a new therapeutic perspective of hepcidin in anti-inflammation in the brain.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
He, Xuan.
Thesis (M.Phil.)--Chinese University of Hong Kong, 2013.
Includes bibliographical references (leaves 110-128).
Abstracts also in Chinese.
ABSTRACT OF THESIS ENTITLED --- p.II
ACKNOWLEDGENENTS --- p.VII
TABLE OF CONTENTS --- p.VIII
LIST OF FIGURES --- p.XII
LIST OF ABBREVIATIONS --- p.XV
Chapter CHAPTER 1 --- INTRODUCTION --- p.1
Chapter 1.1 --- Introductory statement --- p.1
Chapter 1.2 --- Hepcidin in the periphery --- p.1
Chapter 1.2.1 --- Biological functions of hepcidin --- p.3
Chapter 1.2.2 --- Regulation of hepcidin synthesis --- p.10
Chapter 1.2.2.1 --- Regulation of hepcidin by iron --- p.10
Chapter 1.2.2.2 --- Regulation of hepcidin by inflammation --- p.17
Chapter 1.2.2.3 --- Regulation of hepcidin by anemia, erythropoiesis and hypoxia --- p.21
Chapter 1.2.3 --- Misregulation of hepcidin --- p.25
Chapter 1.2.3.1 --- Hepcidin deficiency --- p.25
Chapter 1.2.3.2 --- Hepcidin excess --- p.27
Chapter 1.3 --- Hepcidin in the brain --- p.28
Chapter 1.4 --- Neuroinflammation --- p.30
Chapter 1.5 --- Summary --- p.33
Chapter 1.6 --- Objectives . --- p.34
Chapter CHAPTER 2 --- MATERIALS AND METHODS --- p.36
Chapter 2.1 --- Animal experiments --- p.36
Chapter 2.1.1 --- Intracerebroventricular LPS injection --- p.36
Chapter 2.1.2 --- Animal sacrifice and sample collection --- p.37
Chapter 2.2 --- Cell cultures --- p.38
Chapter 2.2.1 --- Primary cortical neurons culture --- p.38
Chapter 2.2.2 --- BV-2 microglia cells --- p.39
Chapter 2.2.3 --- MES23.5 dopaminergic cells --- p.39
Chapter 2.3 --- Western blot analysis --- p.40
Chapter 2.4 --- ELISA measurement --- p.42
Chapter 2.5 --- Immunohistochemistry --- p.43
Chapter 2.6 --- Statistical analysis --- p.44
Chapter CHAPTER 3 --- IN VIVO STUDY OF THE EFFECTS OF INFLAMMATION ON BRAIN HEPCIDIN EXPRESSION --- p.46
Chapter 3.1 --- ABSTRACT. --- p.46
Chapter 3.2 --- INTRODUCTION --- p.47
Chapter 3.3 --- MATERIALS AND METHODS --- p.48
Chapter 3.4 --- RESULTS --- p.50
Chapter 3.4.1 --- LPS injection induced hepcidin expression in neurons in the cortex and substantia nigra but not in the hippocampus of the rat brain --- p.50
Chapter 3.4.2 --- LPS injection did not induce hepcidin expression in astrocytes in the cortex, hippocampus and substantia nigra of the rat brain --- p.51
Chapter 3.4.3 --- LPS injection induced hepcidin up-regulation and ferroportin down-regulation in the cortex and substantia nigra but not in the hippocampus of the rat brain --- p.52
Chapter 3.4.4 --- LPS injection induced IL-6 production and STAT3 phosphorylation in the cortex, hippocampus and substantia nigra of the rat brain --- p.53
Chapter 3.5 --- DISCUSSION --- p.54
Chapter CHAPTER 4 --- IN VITRO STUDY OF THE MECHANISMS UNDERLYING THE EFFECTS OF INFLAMMATION ON BRAIN HEPCIDIN EXPRESSION --- p.72
Chapter 4.1 --- ABSTRACT --- p.72
Chapter 4.2 --- INTRODUCTION --- p.73
Chapter 4.3 --- MATERIALS AND METHODS --- p.74
Chapter 4.4 --- RESULTS --- p.76
Chapter 4.4.1 --- IL-6 mediated LPS-induced hepcidin expression in primary cortical neurons with the presence of BV-2 microglia --- p.76
Chapter 4.4.2 --- IL-6 induced hepcidin up-regulation and ferroportin down-regulation in primary cortical neurons in an acute manner --- p.77
Chapter 4.4.3 --- Inhibition of STAT3 activity suppressed IL-6-induced hepcidin up-regulation and ferroportin down-regulation in primary cortical neurons --- p.79
Chapter 4.4.4 --- IL-6 rather than other cytokines induced STAT3 activation in primary cortical neurons --- p.80
Chapter 4.4.5 --- Inhibition of STAT3 activity suppressed IL-6-induced hepcidin up-regulation and ferroportin down-regulation in MES23.5 dopaminergic cells --- p.80
Chapter 4.5 --- DISCUSSION --- p.81
Chapter CHAPTER 5 --- GENERAL DISCUSSION --- p.102
REFERENCE --- p.110
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