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Dissertations / Theses on the topic 'Platelet factor 4'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 January 2023

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1

Brousseau-Nault, Mathieu. "Chronic periodontitis is associated with platelet factor 4 (PF4) secretion." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/59016.

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Aim: Platelets contribute to chronic inflammation but their role in periodontitis is not well understood. The aim of this study was to compare platelet recruitment and activation in healthy and inflamed periodontium. Materials and Methods: Gingival crevicular fluid (GCF) samples were obtained from sites of healthy periodontium, gingivitis and periodontitis. Platelets were quantified in the GCF by staining and microscopy. GCF concentrations of platelet factor 4 (PF4) [PF4]GCF and glycoprotein IIbIIIa ([GPIIbIIIa]GCF) were determined by ELISA. Blood samples were obtained from the 3 patient gro
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2

Javaid, Mohammad. "Platelet factor 4 upregulates matrix metalloproteinase-1 production in gingival fibroblasts." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/60244.

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Background and Objective: Periodontitis is a highly prevalent chronic inflammatory disease that causes tooth loss, morbidity and confers an increased risk for systemic disease. Tissue destruction during periodontitis is due in large part to collagen-degrading matrix metalloproteinases (MMPs) released by resident cells of the periodontium in response to pro-inflammatory cytokines. Platelets are immune-competent blood cells with a newly recognized role in chronic inflammation, however their role in the pathogenesis of periodontitis is undefined. Consequently, the objective of this study was to a
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3

Kreimann, Martin [Verfasser]. "Characterization of complexes between platelet factor 4 and heparin / Martin Kreimann." Greifswald : Universitätsbibliothek Greifswald, 2015. http://d-nb.info/1065685513/34.

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4

Yasuba, Hirotaka. "INCREASED RELEASABILITY OF PLATELET PRODUCTS AND REDUCED HEPARIN-INDUCED PLATELET FACTOR 4 RELEASE FROM ENDOTHELIAL CELLS IN BRONCHIAL ASTHMA." Kyoto University, 1991. http://hdl.handle.net/2433/168713.

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本文データは平成22年度国立国会図書館の学位論文(博士)のデジタル化実施により作成された画像ファイルを基にpdf変換したものである<br>Kyoto University (京都大学)<br>0048<br>新制・課程博士<br>医学博士<br>甲第4772号<br>医博第1273号<br>新制||医||500(附属図書館)<br>UT51-91-E143<br>京都大学大学院医学研究科内科系専攻<br>(主査)教授 三河 春樹, 教授 泉 孝英, 教授 大島 駿作<br>学位規則第5条第1項該当
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5

Rudmann, Sally V. "The effect of twenty minutes of aerobic exercise on in vivo platelet release in moderately trained females : radioimmunoassay of platelet factor 4 beta-thromboglobulin /." The Ohio State University, 1986. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487266362337217.

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6

Charpin, Jean-Marie. "Physiopathologie de la bronchiolite obliterante chez les transplantes pulmonaires : implication de 4 mediateurs profibrosants : tgf-beta, igf-1,et-1 et pdgf." Paris 5, 2000. http://www.theses.fr/2000PA05N104.

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7

Etherington, Michael Denis. "An investigation into the measurement of plasma intraplatelet platelet factor 4 and beta-thromboglobulin in health and thrombotic disease." Thesis, University of Southampton, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.278486.

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8

Kimmerle, Sabine. "Rapid determination of Anti-Heparin/Platelet factor 4 antibody titers in the diagnosis of Heparin-induced Thrombocytopenia$cSabine Kimmerle." Bern : [s.n.], 2003. http://www.stub.unibe.ch/html/haupt/datenbanken/diss/bestell.html.

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9

Newman, Peter Michael Pathology UNSW. "Antibody and Antigen in Heparin-Induced Thrombocytopenia." Awarded by:University of New South Wales. Pathology, 2000. http://handle.unsw.edu.au/1959.4/17485.

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Immune heparin-induced thrombocytopenia (HIT) is a potentially serious complication of heparin therapy and is associated with antibodies directed against a complex of platelet factor 4 (PF4) and heparin. Early diagnosis of HIT is important to reduce morbidity and mortality. I developed an enzyme immunoassay that detects the binding of HIT IgG to PF4-heparin in the fluid phase. This required techniques to purify and biotinylate PF4. The fluid phase assay produces consistently low background and can detect low levels of anti-PF4-heparin. It is suited to testing alternative anticoagulants because
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10

Libraire, Julie. "Le facteur 4 plaquettaire (PF4/CXCL4) prévient la formation du complexe initial de l’inhibiteur de l’activateur du plasminogène (PAI-1) avec sa cible d’origine tissulaire (t-PA)." Thesis, Paris 5, 2012. http://www.theses.fr/2012PA05P654.

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Le facteur 4 plaquettaire (PF4/CXCL4) est un tétramère constitué de quatre sous-unités identiques de 7,8 kDa qui est libéré en grande quantité par les plaquettes lors de l’hémostase primaire (ensemble des phénomènes permettant un colmatage initial d’une lésion vasculaire). L’étude de la formation d’un caillot de fibrine en présence de PF4 montre une augmentation de la turbidité finale du caillot : le PF4 modifie le réseau formé. Etant donné que la plupart des acteurs de la fibrinolyse se lie au caillot de fibrine et que le PF4 modifie sa structure, nous avons pensé qu’il serait intéressant de
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11

Santoro, Marcelo Larami. "Contribuição à investigação das alterações hemostáticas induzidas pelo veneno da serpente Bothrops jararaca em coelhos: estudo das glicoproteínas da membrana, função, secreção e sobrevivência plaquetárias." Universidade de São Paulo, 2002. http://www.teses.usp.br/teses/disponiveis/41/41135/tde-17062002-133506/.

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Que o envenenamento pela serpente Bothrops jararaca causa distúrbios hemorrágicos sistêmicos, com alteração da coagulação e fibrinólise sangüíneas, é notório. Contudo, pouco se sabe sobre a ação in vivo desse veneno sobre as plaquetas. Em estudos recentes, demonstrou-se que esse veneno causa trombocitopenia, distúrbios da agregação e diminuição do número de corpos densos plaquetários, que, dessarte, sugeriam a ativação das plaquetas circulantes. Com o escopo de comprovar esta hipótese e melhor caracterizar as ações in vivo desse veneno sobre as plaquetas, serviu-se de um modelo experimental qu
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12

Adenwalla, Nazneen. "Analysis of platelets during malaria infection, and their interaction with Plasmodium-infected erythrocytes." Master's thesis, 2017. http://hdl.handle.net/1885/136517.

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Malaria is an infectious disease caused by Plasmodium parasites, transmitted by the female Anopheles mosquito. Malaria can cause mild symptoms as well as more severe complications which may lead to death. Annually, there are half a million deaths worldwide with millions more newly infected with malaria. Although antimalarials exist, due to the prevalence of drug resistance, novel, more effective treatments are needed to combat malaria by aiding the host immune response. One of the earliest signs of a malarial infection is a decrease in the concentration
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13

Hsiung, Marilyn S. "Mechanisms of D(4) dopamine receptor-mediated platelet-derived growth factor receptor-beta transactivation." 2006. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=442107&T=F.

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14

Chang, Shuyen, and 張淑燕. "The Investigation of the binding of hFGF-1 and platelet factor-4 47-70 peptide." Thesis, 2003. http://ndltd.ncl.edu.tw/handle/79612037033052015885.

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15

Watson, John B. "A structural and functional analysis of Platelet Factor 4 and its interaction with heparan sulfate glycosaminoglycans." 1993. http://catalog.hathitrust.org/api/volumes/oclc/31423439.html.

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16

"Determination of the biological significances of platelet factor 4 (PF4), a tumor suppressor gene encoding an angiogenesis inhibitor in multiple myeloma." 2012. http://library.cuhk.edu.hk/record=b5549446.

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多發性骨髓瘤(Multiple myeloma) 為骨髓內漿細胞異常增生的惡性腫瘤，到目前為止仍然難以治癒。其發生發展是一個複雜的多步驟事件，涉及腫瘤細胞中遺傳和表觀遺傳的改變，以及骨髓微環境的支持。現已確定骨髓瘤細胞和骨髓微環境之間的相互作用對於骨髓瘤的病理發生，以及骨髓瘤細胞的生長，遷移和抗藥性起著關鍵作用。血小根因子四(Platelet factor 4, or PF4) 是一種抗血管生成的趨化因子。它不僅在體外抑制血管內皮細胞增殖和遷移，而且在體內抑制腫瘤的生長。此前，我們發現PF4 基因在多發性骨髓瘤中等位缺失以及DNA 高度甲基化，因而導致其在骨髓瘤病人及細胞系中的表達缺失或降低。在本研究中，我們利用體內和體外實驗鑒定了PF4 對骨髓瘤細胞以及血管生成的作用，並闡明了其作用機制。<br>首先，我們在體外鑒定了PF4 在骨髓瘤細胞中的功能。我們發現PF4 抑制骨髓瘤細胞系以及從病人骨髓中分離出來的骨髓瘤細胞的生長，以及促進其凋亡。其促凋亡活性與caspase-3 和PARP 的激活有關。我們也檢測了PF4 在骨髓瘤中對血管生成的作用。我們首先分離了病人骨髓中的內皮細胞。結果顯示PF4抑制骨髓瘤內皮細胞的生長和管狀物的形成。這些結果證明PF4 在骨髓瘤中可能是一個抑癌因子。<br>接下來我們進一步檢測了PF4 在體內的抑癌功能。在第一種模型中，骨髓瘤細胞被皮下移植到重症聯合
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17

Myler, Heather Ann. "Heparanase and platelet factor-4 induce smooth muscle cell proliferation and migration via basic fibroblast growth factor release from the extracellular matrix: Implications in the restenosis process." Thesis, 2003. http://hdl.handle.net/1911/18597.

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Basic fibroblast growth factor (bFGF) plays an instrumental role in the cascade of events leading to restenosis, vascular re-occlusion due to excessive smooth muscle cell (SMC) proliferation, migration and extracellular matrix (ECM) deposition following arterial intervention procedures such as balloon angioplasty. The mechanism of bFGF activation following vascular injury has remained elusive. bFGF is stored bound to heparan sulfate proteoglycans in the ECM of the arterial media; release from extracellular sequestration may activate bFGF and initiate SMC proliferation and migration. bFGF mobil
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