subject:(plasminogen activator inhibitor 1)

1. Sotiropoulos, Georgios. Ορμόνες του λιπώδους ιστού, φλεγμονώδεις παράγοντες, διαταραχές αιμόστασης και μη μικροκυτταρικός καρκίνος του πνεύμονα.

Degree: 2020, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/47015

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Objectives: Chemerin and PAI-1 are emerging biomarkers at the intersection of inflammation, chemotaxis, thrombosis, fibrinolysis and metabolism. The aims of the present thesis were: 1)… (more)

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Objectives: Chemerin and PAI-1 are emerging biomarkers at the intersection of inflammation, chemotaxis, thrombosis, fibrinolysis and metabolism. The aims of the present thesis were: 1) to explore the association between circulating chemerin and PAI-1 activity in resectable non-small cell lung cancer (NSCLC); 2) to study their diagnostic potential; and 3) to assess their associations with clinicopathological features of NSCLC. Methods: In an adequately powered case-control study, plasma PAI-1 activity, chemerin, metabolic parameters, classic adipokines, hemostatic, inflammatory and tumor biomarkers were measured in 110 consecutive patients with resectable NSCLC and 110 healthy subjects matched on age, sex and date of blood draw.Results: NSCLC patients exhibited significantly higher PAI-1 activity and serum chemerin levels compared to controls (p<0.001). In NSCLC cases, PAI-1 activity correlated with somatometric variables, insulin, WBC, antithrombin III, protein C, plasminogen, IL-6 and tumor size, whereas chemerin with Homeostasis model assessment score of insulin resistance (HOMA-IR), fibrinogen, plasminogen activity, tumor and inflammatory biomarkers, adiponectin, number of infiltrated lymph nodes and NSCLC stage. (p<0.05). Plasma PAI-1 activity and serum chemerin were independently associated with NSCLC beyond and above established risk factors for NSCLC (p<0.001). Plasminogen activity and body mass index emerged as independent predictors of PAI-1 activity in cases, whereas hemostatic parameters (platelet count and plasminogen activity), HOMA-IR, CYFRA 21-1, creatinine and plant food consumption emerged as independent predictors of circulating chemerin (p<0.05). Due to their high specificity, PAI-1 activity and serum chemerin could represent potentially useful parameters in ruling out NSCLC, alone or in combination with serum tumor markers associated with NSCLC. Conclusions: PAI-1 activity and serum chemerin may represent potentially useful biomarkers in NSCLC associated with thrombotic, tumor-promoting and metabolic networks. More clinical studies are needed to explore whether PAI-1 activity and chemerin may be practical biomarkers in the risk assessment of NSCLC at the crossroads of hemostasis, inflammation and metabolism.

Σκοπός: Η χημερίνη και η δραστικότητα του ΡΑΙ-1 αποτελούν ανερχόμενους βιοδείκτες που εμπλέκονται στη φλεγμονή, την πήξη, την ινωδόλυση και τον μεταβολισμό. Σκοπός αυτή της διδακτορικής διατριβής ήταν: 1) η διερεύνηση της σχέσης του ΡΑΙ-1 και της χημερίνης με τον ΜΜΚΠ, 2) η διερεύνηση της διαγνωστικής τους αξίας,3) η διερεύνηση της συσχέτισής τους με κλινικοπαθλογικά χαρακτηριστικά της νόσου. Υλικό και Μέθοδος: Σε μία μελέτη τύπου ασθενών-μαρτύρων, με επαρκή στατιστική ισχύ, μετρήθηκαν η χημερίνη, η δραστικότητα του ΡΑΙ-1, οι μεταβολικοί παράγοντες, οι κλασσικές λιποκίνες,οι αιμοστατικοί, φλεγμονώδεις και καρκινικοί βιοδείκτες σε 110 διαδοχικούς ασθενείς με νεοδιαγνωσθέν ΜΜΚΠ και σε 110 υγιείς μάρτυρες, εξομοιωμένους ως προς την ηλικία, το φύλο και την ημερομηνία αιμοληψίας.…

Subjects/Keywords: Χημερίνη; ΜΜΚΠ; Plasminogen activator inhibitor-1 (PAI-1)

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sotiropoulos, G. (2020). Ορμόνες του λιπώδους ιστού, φλεγμονώδεις παράγοντες, διαταραχές αιμόστασης και μη μικροκυτταρικός καρκίνος του πνεύμονα. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/47015

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Sotiropoulos, Georgios. “Ορμόνες του λιπώδους ιστού, φλεγμονώδεις παράγοντες, διαταραχές αιμόστασης και μη μικροκυτταρικός καρκίνος του πνεύμονα.” 2020. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed April 16, 2021. http://hdl.handle.net/10442/hedi/47015.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Sotiropoulos, Georgios. “Ορμόνες του λιπώδους ιστού, φλεγμονώδεις παράγοντες, διαταραχές αιμόστασης και μη μικροκυτταρικός καρκίνος του πνεύμονα.” 2020. Web. 16 Apr 2021.

Vancouver:

Sotiropoulos G. Ορμόνες του λιπώδους ιστού, φλεγμονώδεις παράγοντες, διαταραχές αιμόστασης και μη μικροκυτταρικός καρκίνος του πνεύμονα. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2020. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/10442/hedi/47015.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Sotiropoulos G. Ορμόνες του λιπώδους ιστού, φλεγμονώδεις παράγοντες, διαταραχές αιμόστασης και μη μικροκυτταρικός καρκίνος του πνεύμονα. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2020. Available from: http://hdl.handle.net/10442/hedi/47015

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Vanderbilt University

2. White, Marquitta Jonisse. Genetics of Plasminogen Activator Inhibitor – 1: a potent biological effector of cardiovascular disease risk.

Degree: PhD, Human Genetics, 2014, Vanderbilt University

URL: http://hdl.handle.net/1803/14029

► Cardiovascular disease (CVD) is an inclusive term encompassing several disorders of the circulatory system that together account for the majority of global non-communicable disease (NCD)… (more)

▼ Cardiovascular disease (CVD) is an inclusive term encompassing several disorders of the circulatory system that together account for the majority of global non-communicable disease (NCD) mortality. Major thrombotic events, due in part to impaired fibrinolysis, are a unifying characteristic of several CVDs. Plasminogen activator inhibitor-1 (PAI-1) is a major regulator of fibrinolysis, and PAI-1 levels associate with CVD susceptibility and severity in several populations. The main objectives of this dissertation were to evaluate the genetic impact of common single nucleotide polymorphisms (SNPs) on inter-individual variation in PAI-1 levels in a Ghanaian population, and present a novel method to identify candidate genes for prioritization in future studies. We discovered novel associations between single variants in the arylsulfatase b (ARSB), carboxypeptidase A2 (CPA2), and leukocyte receptor cluster member 9 (LENG9) and median PAI-1 levels. Quantile regression analyses directed at the upper quartile of the PAI-1 distribution was performed to uncover novel variants with significant impact on this clinically relevant portion of the PAI-1 distribution. Upper quartile regression analyses revealed significant associations between single variants in period circadian clock 3 (PER3), a discovery that supports previous evidence of the involvement of the circadian pathway in regulation of PAI-1 levels in Caucasian populations as well as model organisms. This finding suggests that the significance of the circadian pathway as a whole may be generalizable across populations, even though gene effects may be population specific. We present a novel approach; Multi-lOcus based selection of Candidate genes (MOCA), which incorporates multi-variant association signals into the prioritization of genes for further evaluation. MOCA identified four significantly associated loci; these loci included 28 novel candidate genes for PAI-1 levels. Each MOCA identified locus was located within previously identified CVD and/or PAI-1 related quantitative trait loci (QTL). Advisors/Committee Members: Nancy J. Brown (committee member), melinda aldrich (committee member), Dana Crawford (committee member), Jason Moore (committee member), Scott M. Williams (committee member), Bingshan Li (Committee Chair).

Subjects/Keywords: population genetics; plasminogen activator inhibitor-1; cardiovascular disease

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

White, M. J. (2014). Genetics of Plasminogen Activator Inhibitor – 1: a potent biological effector of cardiovascular disease risk. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14029

Chicago Manual of Style (16^th Edition):

White, Marquitta Jonisse. “Genetics of Plasminogen Activator Inhibitor – 1: a potent biological effector of cardiovascular disease risk.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed April 16, 2021. http://hdl.handle.net/1803/14029.

MLA Handbook (7^th Edition):

White, Marquitta Jonisse. “Genetics of Plasminogen Activator Inhibitor – 1: a potent biological effector of cardiovascular disease risk.” 2014. Web. 16 Apr 2021.

Vancouver:

White MJ. Genetics of Plasminogen Activator Inhibitor – 1: a potent biological effector of cardiovascular disease risk. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1803/14029.

Council of Science Editors:

White MJ. Genetics of Plasminogen Activator Inhibitor – 1: a potent biological effector of cardiovascular disease risk. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/14029

University of Manitoba

3. Sangle, Ganesh. Mechanisms for Oxidized or Glycated LDL-induced Oxidative Stress and Upregulation of Plasminogen Activator Inhibitor-1 in Vascular Cells.

Degree: Physiology, 2010, University of Manitoba

URL: http://hdl.handle.net/1993/4185

► Atherosclerotic cardiovascular disease is the leading cause of death of adults in North America. Diabetes is a classical risk factor for atherosclerotic cardiovascular disease. Plasminogen… (more)

▼ Atherosclerotic cardiovascular disease is the leading cause of death of adults in North America. Diabetes is a classical risk factor for atherosclerotic cardiovascular disease. Plasminogen activator inhibitor-1 (PAI-1) is the major physiological inhibitor of fibrinolysis. Elevated levels of PAI-1, oxidized low-density lipoprotein (oxLDL) and glycated LDL (glyLDL) were detected in patients with diabetes. Increased oxidative stress is associated with diabetic cardiovascular complications. Previous studies in our laboratory demonstrated that oxLDL or glyLDL increased the production of PAI-1 or reactive oxygen species (ROS) in vascular endothelial cells (EC). This study was undertaken to investigate transmembrane signaling mechanisms involved in oxLDL or glyLDL-induced upregulation of PAI-1 in cultured vascular EC. Further, we examined the mechanism for oxLDL or glyLDL-induced oxidative stress in EC. The results of the present studies demonstrated novel transmembrane signaling pathway for oxLDL-induced PAI-1 production in vascular EC. We demonstrated that lectin-like oxLDL receptor-1, H-Ras, a small G-protein and Raf-1/ERK-1/2 mediate oxLDL-induced PAI-1 expression in cultured EC. GlyLDL may activate EC via a distinct transmembrane signaling pathway. The results of the present study demonstrated that receptor for advanced glycation end products, NADPH oxidase and H-Ras/Raf-1 are implicated in the upregulation of heat shock factor-1 or PAI-1 in vascular EC under diabetes-associated metabolic stress. We investigated the effects of oxLDL or glyLDL on mitochondrial function in EC. Treatment with oxLDL or glyLDL significantly impaired the activities of electron transport chain (ETC) enzymes and also increased mitochondria-associated ROS in EC. The findings suggest that oxLDL or glyLDL attenuated activity of ETC and increased ROS generation in EC, which potentially contributes to oxidative stress in vasculature. In conclusion, diabetes-associated lipoproteins may upregulate stress response mediators and PAI-1 production via distinct transmembrane signaling pathways. OxLDL or glyLDL may increase ROS production via NOX activation and the impairment of mitochondrial ETC enzyme activity in EC. The understanding and identification of the regulatory mechanisms involved in diabetes-associated lipoprotein-induced signaling may help pharmacological design for the management of diabetic cardiovascular complications. Advisors/Committee Members: Shen, Garry (Internal Medicine) (supervisor), Halayko, Andrew (Physiology) Nyomba, Gregoire (Internal Medicine) Moghadasian, Mohammed (Human Nutritional Sciences) Chakrabarti, Subrata (University of Western Ontario) (examiningcommittee).

Subjects/Keywords: Plasminogen activator inhibitor-1; Atherosclerosis; glycated LDL; oxidized LDL; diabetes

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sangle, G. (2010). Mechanisms for Oxidized or Glycated LDL-induced Oxidative Stress and Upregulation of Plasminogen Activator Inhibitor-1 in Vascular Cells. (Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/4185

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Sangle, Ganesh. “Mechanisms for Oxidized or Glycated LDL-induced Oxidative Stress and Upregulation of Plasminogen Activator Inhibitor-1 in Vascular Cells.” 2010. Thesis, University of Manitoba. Accessed April 16, 2021. http://hdl.handle.net/1993/4185.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Sangle, Ganesh. “Mechanisms for Oxidized or Glycated LDL-induced Oxidative Stress and Upregulation of Plasminogen Activator Inhibitor-1 in Vascular Cells.” 2010. Web. 16 Apr 2021.

Vancouver:

Sangle G. Mechanisms for Oxidized or Glycated LDL-induced Oxidative Stress and Upregulation of Plasminogen Activator Inhibitor-1 in Vascular Cells. [Internet] [Thesis]. University of Manitoba; 2010. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1993/4185.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Sangle G. Mechanisms for Oxidized or Glycated LDL-induced Oxidative Stress and Upregulation of Plasminogen Activator Inhibitor-1 in Vascular Cells. [Thesis]. University of Manitoba; 2010. Available from: http://hdl.handle.net/1993/4185

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Southern California

4. Fang, Hua. Targeting BCL-2 family proteins and plasminogen activator inhibitor-1 in turmor cell apoptosis.

Degree: Doctor of Medicine, Pathobiology, 2012, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/33557/rec/6323

► Resistance to cell death, especially to apoptosis, is an important feature of tumor cells, which is also described as one of the hallmarks in cancer.… (more)

Subjects/Keywords: apoptosis; Bcl-2; ABT-737; plasminogen activator inhibitor-1; cancer

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Fang, H. (2012). Targeting BCL-2 family proteins and plasminogen activator inhibitor-1 in turmor cell apoptosis. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/33557/rec/6323

Chicago Manual of Style (16^th Edition):

Fang, Hua. “Targeting BCL-2 family proteins and plasminogen activator inhibitor-1 in turmor cell apoptosis.” 2012. Doctoral Dissertation, University of Southern California. Accessed April 16, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/33557/rec/6323.

MLA Handbook (7^th Edition):

Fang, Hua. “Targeting BCL-2 family proteins and plasminogen activator inhibitor-1 in turmor cell apoptosis.” 2012. Web. 16 Apr 2021.

Vancouver:

Fang H. Targeting BCL-2 family proteins and plasminogen activator inhibitor-1 in turmor cell apoptosis. [Internet] [Doctoral dissertation]. University of Southern California; 2012. [cited 2021 Apr 16]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/33557/rec/6323.

Council of Science Editors:

Fang H. Targeting BCL-2 family proteins and plasminogen activator inhibitor-1 in turmor cell apoptosis. [Doctoral Dissertation]. University of Southern California; 2012. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/33557/rec/6323

Kyoto University

5. Miyazaki, Hiroshi. Studies on Inhibitors of Plasminogen Activator Inhibitor-1(PAI-1) and Inhibitors of PAI-1 Production as Antithrombotic Agents .

Degree: 2010, Kyoto University

URL: http://hdl.handle.net/2433/126818

Subjects/Keywords: Plasminogen Activator inhibitor-1; PAI-1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Miyazaki, H. (2010). Studies on Inhibitors of Plasminogen Activator Inhibitor-1(PAI-1) and Inhibitors of PAI-1 Production as Antithrombotic Agents . (Thesis). Kyoto University. Retrieved from http://hdl.handle.net/2433/126818

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Miyazaki, Hiroshi. “Studies on Inhibitors of Plasminogen Activator Inhibitor-1(PAI-1) and Inhibitors of PAI-1 Production as Antithrombotic Agents .” 2010. Thesis, Kyoto University. Accessed April 16, 2021. http://hdl.handle.net/2433/126818.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Miyazaki, Hiroshi. “Studies on Inhibitors of Plasminogen Activator Inhibitor-1(PAI-1) and Inhibitors of PAI-1 Production as Antithrombotic Agents .” 2010. Web. 16 Apr 2021.

Vancouver:

Miyazaki H. Studies on Inhibitors of Plasminogen Activator Inhibitor-1(PAI-1) and Inhibitors of PAI-1 Production as Antithrombotic Agents . [Internet] [Thesis]. Kyoto University; 2010. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/2433/126818.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Miyazaki H. Studies on Inhibitors of Plasminogen Activator Inhibitor-1(PAI-1) and Inhibitors of PAI-1 Production as Antithrombotic Agents . [Thesis]. Kyoto University; 2010. Available from: http://hdl.handle.net/2433/126818

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Freie Universität Berlin

6. Bukreeva, Larisa. Studies on the relationship of plasminogen activator inhibitor-1 for venous thromboembolism.

Degree: 2013, Freie Universität Berlin

URL: http://dx.doi.org/10.17169/refubium-12047

► Venous thromboembolism (VTE) is a chronic multifactorial disease with expositional and dispositional risk factors. The established risk factors include deficiency of antithrombin, protein C and… (more)

Subjects/Keywords: venous thromboembolism; plasminogen activator inhibitor-1; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Bukreeva, L. (2013). Studies on the relationship of plasminogen activator inhibitor-1 for venous thromboembolism. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-12047

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Bukreeva, Larisa. “Studies on the relationship of plasminogen activator inhibitor-1 for venous thromboembolism.” 2013. Thesis, Freie Universität Berlin. Accessed April 16, 2021. http://dx.doi.org/10.17169/refubium-12047.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Bukreeva, Larisa. “Studies on the relationship of plasminogen activator inhibitor-1 for venous thromboembolism.” 2013. Web. 16 Apr 2021.

Vancouver:

Bukreeva L. Studies on the relationship of plasminogen activator inhibitor-1 for venous thromboembolism. [Internet] [Thesis]. Freie Universität Berlin; 2013. [cited 2021 Apr 16]. Available from: http://dx.doi.org/10.17169/refubium-12047.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Bukreeva L. Studies on the relationship of plasminogen activator inhibitor-1 for venous thromboembolism. [Thesis]. Freie Universität Berlin; 2013. Available from: http://dx.doi.org/10.17169/refubium-12047

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

7. V. DE LORENZI. CROSS-TALK BETWEEN THE PROTEOLYTIC AND NON-PROTEOLYTIC FUNCTIONS OF THE UROKINASE RECEPTOR.

Degree: 2015, Università degli Studi di Milano

URL: http://hdl.handle.net/2434/265507

► Urokinase (uPA) and its cell surface receptor (uPAR) have been implicated in a wide variety of biological processes related to tissue homeostasis. Moreover the uPA-system… (more)

▼ Urokinase (uPA) and its cell surface receptor (uPAR) have been implicated in a wide variety of biological processes related to tissue homeostasis. Moreover the uPA-system plays an important role in many pathological events, such as tumour cell migration and dissemination. On the one hand, the binding of uPA to uPAR favours extracellular proteolysis by enhancing cell surface plasminogen activation. On the other hand, it promotes cell adhesion and signalling through binding of the provisional matrix protein vitronectin (VN). Although the existence of feedback loops between the functions of uPAR in extracellular proteolysis, cell adhesion and signalling has been described, some aspects of this cross-talk are still poorly understood and not characterized experimentally. We here report that cell surface plasminogen activation induces a potent negative feedback on cell adhesion to VN. The feedback is predominantly caused by proteolytic cleavage of the RGD-motif in VN catalyzed by both uPA and plasmin. In this process the cell-adhesive properties of VN are impaired by disruption of the integrin binding site and release of the somatomedin B (SMB) domain responsible for binding of uPAR. Cleavage of VN by uPA displays a remarkable receptor-dependence and requires concomitant binding of both uPA and VN to uPAR suggesting that the hydrolysis is accelerated by a mechanism of substrate presentation. VN represents the first described uPAR-dependent substrate of uPA and our findings therefore identify a potential novel function of uPAR in focusing the proteolytic activity of the plasminogen activation system onto extracellular matrix-associated VN. Additionally, SMB-containing N-terminal VN fragments are released by several cancer cell lines in vitro and are detectable in human urines samples. We have thus developed a clinical grade immunoassay for the detection and quantification of such fragments in urine samples with the aim of using the levels of urinary VN fragments as a novel cancer biomarker. Our working hypothesis is that this biomarker may be used as an indirect functional measurement of the uPA-system activity in the tumour tissue. Finally, we show that the specific urokinase inhibitor, plasminogen activator inhibitor 1 (PAI-1), blocks the negative feedback mediated by uPA and behaves as a potent uPA-dependent agonist of the interaction between uPAR and VN. Indeed, we report for the first time that the covalent complex between uPA and PAI-1 is endowed with higher agonistic activity compared to uPA. Taken together, these data might represent a molecular explanation of the poor clinical outcome observed in cancer patients with high levels of uPA and PAI-1. Advisors/Committee Members: internal advisor: G. Scita, external advisor: V. Ellis, supervisor: N. Sidenius.

Subjects/Keywords: extracellular proteolysis; urokinase receptor; vitronectin; plasminogen activation; plasminogen activator inhibitor-1; biomarker; cell adhesion; Settore BIO/10 - Biochimica

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

LORENZI, V. D. (2015). CROSS-TALK BETWEEN THE PROTEOLYTIC AND NON-PROTEOLYTIC FUNCTIONS OF THE UROKINASE RECEPTOR. (Thesis). Università degli Studi di Milano. Retrieved from http://hdl.handle.net/2434/265507

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

LORENZI, V. DE. “CROSS-TALK BETWEEN THE PROTEOLYTIC AND NON-PROTEOLYTIC FUNCTIONS OF THE UROKINASE RECEPTOR.” 2015. Thesis, Università degli Studi di Milano. Accessed April 16, 2021. http://hdl.handle.net/2434/265507.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

LORENZI, V. DE. “CROSS-TALK BETWEEN THE PROTEOLYTIC AND NON-PROTEOLYTIC FUNCTIONS OF THE UROKINASE RECEPTOR.” 2015. Web. 16 Apr 2021.

Vancouver:

LORENZI VD. CROSS-TALK BETWEEN THE PROTEOLYTIC AND NON-PROTEOLYTIC FUNCTIONS OF THE UROKINASE RECEPTOR. [Internet] [Thesis]. Università degli Studi di Milano; 2015. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/2434/265507.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

LORENZI VD. CROSS-TALK BETWEEN THE PROTEOLYTIC AND NON-PROTEOLYTIC FUNCTIONS OF THE UROKINASE RECEPTOR. [Thesis]. Università degli Studi di Milano; 2015. Available from: http://hdl.handle.net/2434/265507

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Vienna

8. Jauernegger, Renate. Investigation of biomarkers associated with the fibrinolytic system in plasma and CSF of patients with MS.

Degree: 2018, University of Vienna

URL: http://othes.univie.ac.at/55658/

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Multiple Sklerose ist eine der häufigsten neurologischen Erkrankungen in jungen Erwachsenen und man nimmt an, dass unter anderem ein Zusammenbruch der Bluthirnschranke und Eintritt von… (more)

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Multiple Sklerose ist eine der häufigsten neurologischen Erkrankungen in jungen Erwachsenen und man nimmt an, dass unter anderem ein Zusammenbruch der Bluthirnschranke und Eintritt von Plasmaproteinen für die Neurodegeneration verantwortlich sind. In unserem Projekt wurden daher Plasma und CSF Proben von MS-Patienten und Patienten mit anderen neurologischen Störungen untersucht. Mittels ELISAs wurden Fibrinogen, Plasminogen, a2-Antiplasmin und tPA:PAI1 Komplex in den Plasma und CSF Proben quantifiziert und die Ergebnisse mit Graphpad Prism 7 ausgewertet. Erwartete erhöhte Proteinkonzentrationen und signifikante Unterschiede zwischen MS und nicht-MS Patienten konnten nicht bestätigt werden. Quantifizierbare Proteinkonzentrationen im CSF von beiden Patientengruppen lassen auf eine beschädigte Blut-Hirn-Schranke in neurologischen Erkrankungen schließen. Zusätzlich wurde ein umgekehrtes Verhältnis von Plasminogen:a2-Antiplasmin im CSF beider Patientengruppen gefunden. Dieses Verhältnis spielt möglicherweise eine Rolle in neurologischen Erkrankungen, welche genau ist aber noch unklar und bedarf weiterer Forschung.

Multiple sclerosis is one of the major causes for neurological diseases in young adults. It`s pathogenetic mechanisms are still not completely understood but it seems that disruption of the blood-brain barrier and entering of plasma proteins play a vital role in disease onset and exacerbation. Hence our project focused on the investigation of biomarkers associated with the fibrinolytic system in plasma and CSF samples of patients with MS and other neurological diseases. ELISAs were used to quantify fibrinogen, plasminogen, a2-antiplasmin and tPA:PAI1 complex in plasma and CSF samples. Unexpectedly there was no significant elevation of protein levels in the MS-group compared to the non-MS group. However, detectable protein levels in the CSF of both patient groups seem to confirm a disrupted brain barrier in neurological diseases. We found a reversed plasminogen-a2-antiplasmin-ratio in the CSF of both patient groups. This may suggest a role for the fibrinolytic system in neurological diseases. However, further investigation is still needed.

Subjects/Keywords: 44.38 Pharmakologie; 44.90 Neurologie; Multiple Sklerose / Blut-Hirn-Schranke / Fibrinogen / Plasminogen / Plasminogen-Aktivator-Inhibitor-1 / a2-Antiplasmin / Gewebespezifischer Plasminogenaktivator / ELISA / Protein Konzentration; multiple sclerois / blood-brain-barrier / fibrinogen / plasminogen / plasminogen-activator-inhibitor-1 / a2-antiplasmin / tissue plasminogen activator / ELISA / protein levels

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Jauernegger, R. (2018). Investigation of biomarkers associated with the fibrinolytic system in plasma and CSF of patients with MS. (Thesis). University of Vienna. Retrieved from http://othes.univie.ac.at/55658/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Jauernegger, Renate. “Investigation of biomarkers associated with the fibrinolytic system in plasma and CSF of patients with MS.” 2018. Thesis, University of Vienna. Accessed April 16, 2021. http://othes.univie.ac.at/55658/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Jauernegger, Renate. “Investigation of biomarkers associated with the fibrinolytic system in plasma and CSF of patients with MS.” 2018. Web. 16 Apr 2021.

Vancouver:

Jauernegger R. Investigation of biomarkers associated with the fibrinolytic system in plasma and CSF of patients with MS. [Internet] [Thesis]. University of Vienna; 2018. [cited 2021 Apr 16]. Available from: http://othes.univie.ac.at/55658/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Jauernegger R. Investigation of biomarkers associated with the fibrinolytic system in plasma and CSF of patients with MS. [Thesis]. University of Vienna; 2018. Available from: http://othes.univie.ac.at/55658/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

9. 三上,大輔. Telmisartan activates endogenous peroxisome proliferator-activated receptor-δ and may have anti-fibrotic effects in human mesangial cells : テルミサルタンはヒトメサンギウム細胞において，内因性peroxisome proliferator-activated receptor-δ(PPAR-δ)を活性化し，潜在的な抗線維化作用を有する.

Degree: 博士(医学）, University of Fukui / 福井大学

URL: http://hdl.handle.net/10098/8448

以下に掲載：Hypertension Research 37 pp.422-431 2014. Nature Publishing Group. 共著者：Hideki Kimura, Kazuko Kamiyama, Kunio Torii, Kenji Kasuno, Naoki Takahashi, Haruyoshi Yoshida, Masayuki Iwano

Subjects/Keywords: ERK pathway; plasminogen activator inhibitor-1; TGF-beta 1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

三上,大輔. (n.d.). Telmisartan activates endogenous peroxisome proliferator-activated receptor-δ and may have anti-fibrotic effects in human mesangial cells : テルミサルタンはヒトメサンギウム細胞において，内因性peroxisome proliferator-activated receptor-δ(PPAR-δ)を活性化し，潜在的な抗線維化作用を有する. (Thesis). University of Fukui / 福井大学. Retrieved from http://hdl.handle.net/10098/8448

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

三上,大輔. “Telmisartan activates endogenous peroxisome proliferator-activated receptor-δ and may have anti-fibrotic effects in human mesangial cells : テルミサルタンはヒトメサンギウム細胞において，内因性peroxisome proliferator-activated receptor-δ(PPAR-δ)を活性化し，潜在的な抗線維化作用を有する.” Thesis, University of Fukui / 福井大学. Accessed April 16, 2021. http://hdl.handle.net/10098/8448.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

三上,大輔. “Telmisartan activates endogenous peroxisome proliferator-activated receptor-δ and may have anti-fibrotic effects in human mesangial cells : テルミサルタンはヒトメサンギウム細胞において，内因性peroxisome proliferator-activated receptor-δ(PPAR-δ)を活性化し，潜在的な抗線維化作用を有する.” Web. 16 Apr 2021.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
No year of publication.

Vancouver:

三上,大輔. Telmisartan activates endogenous peroxisome proliferator-activated receptor-δ and may have anti-fibrotic effects in human mesangial cells : テルミサルタンはヒトメサンギウム細胞において，内因性peroxisome proliferator-activated receptor-δ(PPAR-δ)を活性化し，潜在的な抗線維化作用を有する. [Internet] [Thesis]. University of Fukui / 福井大学; [cited 2021 Apr 16]. Available from: http://hdl.handle.net/10098/8448.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Council of Science Editors:

三上,大輔. Telmisartan activates endogenous peroxisome proliferator-activated receptor-δ and may have anti-fibrotic effects in human mesangial cells : テルミサルタンはヒトメサンギウム細胞において，内因性peroxisome proliferator-activated receptor-δ(PPAR-δ)を活性化し，潜在的な抗線維化作用を有する. [Thesis]. University of Fukui / 福井大学; Available from: http://hdl.handle.net/10098/8448

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

University of Michigan

10. Huttinger, Zachary. Functional Characterization of Fibrinolysis-Modulating Proteins Using High Throughput Phage Display.

Degree: PhD, Cellular & Molec Biology PhD, 2020, University of Michigan

URL: http://hdl.handle.net/2027.42/155177

► The advent of modern high throughput sequencing (HTS) technology has resulted in the resurgence of phage display as a powerful technique in screening peptide and… (more)

▼ The advent of modern high throughput sequencing (HTS) technology has resulted in the resurgence of phage display as a powerful technique in screening peptide and protein libraries for mutations and/or protein fragments with desired properties. As the protein or peptide is covalently tethered to (or “displayed” on) the surface of the bacteriophage, its corresponding genetic material may be rapidly identified and analyzed using DNA sequencing technologies. As the earliest applications of phage display were limited by the available methods (low-throughput Sanger DNA sequencing), repetitive rounds of selection and amplification were required, and only a small portion of the selected phage could be analyzed. Coupling phage display with HTS creates a new high throughput platform, termed high throughput phage display, with which to quickly and without bias screen vast libraries of peptides and proteins for novel binding interactions, stability, and kinetics. High throughput phage display allows characterization of the population of a library of >106 phage prior to and after selection to determine the level of enrichment or depletion of individual clones within the library. In this dissertation, I will highlight the potential of high throughput phage display with two different yet complimentary applications: Streptococcus pyogenes (GAS) is a pathogenic bacteria that activates the fibrinolytic system via a secreted virulence factor, streptokinase, facilitating GAS dissemination throughout the human host and evasion of the host immune system. A small, bioactive compound that inhibits streptokinase expression was previously developed and validated in a humanized mouse model of GAS septicemia. The mechanism of action and target of the compound within GAS remain unknown. A candidate gene was ruled out using genetic studies so an unbiased biochemical approach to identify GAS proteins involved in its mechanism of action was undertaken. Randomly fragmented GAS genomic DNA was cloned into a phage display vector in order to create a library of phage displaying GAS peptides on their surface. Although the utility of this library was hindered by technical difficulties during preparation, it demonstrated feasibility of constructing large and diverse phage display libraries that could be useful in other applications. As a serine protease inhibitor (serpin), plasminogen activator inhibitor-1 (PAI-1) regulates the fibrinolytic system by inhibiting the plasminogen activators, tissue-type and urokinase-type plasminogen activator PAI-1 undergoes spontaneous conformational conversion to an inactive, latent state with a half-life of 2 hours. Two previous whole gene mutagenesis studies identified mutations that stabilize the active conformation of PAI-1 but ultimately only characterized the effects of 1.2% of all possible amino acid substitutions on PAI-1 stability. Here we report the construction and screening of a phage display library of PAI-1 variants to examine the mutational landscape with respect to functional stability. Using high… Advisors/Committee Members: Ginsburg, David (committee member), Sandkvist, Maria B (committee member), Lawrence, Daniel Allen (committee member), Shavit, Jordan A (committee member).

Subjects/Keywords: PAI-1; Plasminogen activator inhibitor-1; Phage Display; High Throughput Sequencing; Biological Chemistry; Molecular, Cellular and Developmental Biology; Health Sciences

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Huttinger, Z. (2020). Functional Characterization of Fibrinolysis-Modulating Proteins Using High Throughput Phage Display. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/155177

Chicago Manual of Style (16^th Edition):

Huttinger, Zachary. “Functional Characterization of Fibrinolysis-Modulating Proteins Using High Throughput Phage Display.” 2020. Doctoral Dissertation, University of Michigan. Accessed April 16, 2021. http://hdl.handle.net/2027.42/155177.

MLA Handbook (7^th Edition):

Huttinger, Zachary. “Functional Characterization of Fibrinolysis-Modulating Proteins Using High Throughput Phage Display.” 2020. Web. 16 Apr 2021.

Vancouver:

Huttinger Z. Functional Characterization of Fibrinolysis-Modulating Proteins Using High Throughput Phage Display. [Internet] [Doctoral dissertation]. University of Michigan; 2020. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/2027.42/155177.

Council of Science Editors:

Huttinger Z. Functional Characterization of Fibrinolysis-Modulating Proteins Using High Throughput Phage Display. [Doctoral Dissertation]. University of Michigan; 2020. Available from: http://hdl.handle.net/2027.42/155177

11. Sokolakis, Thomas. Διαβητική αμφιβληστροειδοπάθεια σε Έλληνες καυκάσιους πάσχοντες από διαβήτη τύπου 2, συσχέτιση με τον πολυμορφισμό στο γονίδιο του αναστολέα του ενεργοποιητή του πλασμινογόνου 1 (ΡAI 1).

Degree: 2017, University of Thessaly (UTH); Πανεπιστήμιο Θεσσαλίας

URL: http://hdl.handle.net/10442/hedi/42107

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Background: There is accumulating evidence for genetic susceptibility to the development of diabetic retinopathy (DR). The role of plasminogen activator inhibitor-1 (PAI-1) in DR risk… (more)

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Background: There is accumulating evidence for genetic susceptibility to the development of diabetic retinopathy (DR). The role of plasminogen activator inhibitor-1 (PAI-1) in DR risk remains controversial.Objective: The present study was designed to investigate possible influence of PAI-1 gene region polymorphisms on the risk of DR and on the risk of developing DR early vs late in the course of type 2 diabetes mellitus (T2DM).Methods: A total of 138 patients with DR, 107 patients with T2DM without DR, and 315 healthy controls were recruited. To cover the majority of the genetic variability across the extended region of PAI-1 gene, five tag single-nucleotide polymorphisms (SNPs) from the HapMap using a pairwise approach and an r2 ≥ 0.8 and a minor allele frequency (MAF) of >0.05 were identified. Using logistic regression analyses, tag SNPs and haplotypes were tested for associations with DR risk and risk of DR development early or late in the course of T2DM. The generalized odds ratio (ORG) was calculated to estimate the mutational load effect on DR development among all participants. Corrections for multiple comparisons were carried out (p-value < 0.01).Results: A significant effect of rs2070682 on the risk of early DR onset was found in the codominant model of inheritance [odds ratio, OR (95% confidence interval, CI): 5.04 (1.47–17.28), p = 0.018]. However, this association marginally did not survive multiple testing corrections. No other significant association between PAI-1 tag-SNPs and haplotypes was revealed. Furthermore, no significant mutational load effect of PAI-1 tag SNPs on the risk of DR development in T2DM course was found.Conclusions: In conclusion, the present study does not provide any strong evidence that PAI-1 gene variants are implicated in the risk of DR or the development of DR during T2DM course.

Ιστορικό: Υπαρχουν συσσωρεύμενα στοιχεία για την ύπαρξη γενετικής ευαισθησίας στην ανάπτυξη διαβητικής αμφιβληστροειδοπάθειας (ΔΑ). Ο ρόλος του αναστολέα του ενεργοποιητή του πλασμινογόνου-1 (PAI-1) στον κινδυνο αναπτυξης ΔΑ παραμένει αμφιλεγόμενος.Σκοπός: Η παρούσα μελέτη σχεδιάστηκε για να διερευνήσει την πιθανή επίδραση των πολυμορφισμών της περιοχής του γονιδίου PAI-1 στον κίνδυνο ανάπτυξης της ΔΑ και στον κίνδυνο ανάπτυξης ΔΑ πρώιμα έναντι καθυστερημένα κατά τη διάρκεια του σακχαρώδους διαβήτη τύπου 2 (ΣΔ2). Μέθοδοι: Συνολικά 138 ασθενείς με ΔΑ, 107 ασθενείς με ΣΔ2 χωρίς ΔΑ και 315 υγιείς μάρτυρες προσλήφθηκαν. Για να καλυφθεί η πλειοψηφία της γενετικής μεταβλητότητας στην εκτεταμένη περιοχή του γονιδίου ΡΑΙ-1, πέντε πολυμορφισμοί μονού νουκλεοτιδίου (single-nucleotide polymorphisms SNPs) από το HapMap χρησιμοποιώντας μια προσέγγιση ανά ζεύγη και r2> 0,8 και μία μικρή συχνότητα αλληλόμορφων (minor allele frequency MAF)> 0,05 εντοπίστηκαν. Χρησιμοποιώντας αναλύσεις λογιστικής παλινδρόμησης, ετικέτες SNPs και απλότυποι δοκιμάστηκαν για ενώσεις με κίνδυνο ανάπτυξης ΔΑ και με κίνδυνο ανάπτυξης ΔΑ νωρίς ή αργά κατά τη διάρκεια του ΣΔ2. Ο γενικευμένος λόγος πιθανότητας (generalized odds ratio ORG)…

Subjects/Keywords: Διαβητική αμφιβληστροειδοπάθεια; Πολυμορφισμός στο γονίδιο του αναστολέα του ενεργοποιητή του πλασμινογόνου 1; Diabetic retinopathy; Plasminogen activator inhibitor 1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sokolakis, T. (2017). Διαβητική αμφιβληστροειδοπάθεια σε Έλληνες καυκάσιους πάσχοντες από διαβήτη τύπου 2, συσχέτιση με τον πολυμορφισμό στο γονίδιο του αναστολέα του ενεργοποιητή του πλασμινογόνου 1 (ΡAI 1). (Thesis). University of Thessaly (UTH); Πανεπιστήμιο Θεσσαλίας. Retrieved from http://hdl.handle.net/10442/hedi/42107

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Sokolakis, Thomas. “Διαβητική αμφιβληστροειδοπάθεια σε Έλληνες καυκάσιους πάσχοντες από διαβήτη τύπου 2, συσχέτιση με τον πολυμορφισμό στο γονίδιο του αναστολέα του ενεργοποιητή του πλασμινογόνου 1 (ΡAI 1).” 2017. Thesis, University of Thessaly (UTH); Πανεπιστήμιο Θεσσαλίας. Accessed April 16, 2021. http://hdl.handle.net/10442/hedi/42107.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Sokolakis, Thomas. “Διαβητική αμφιβληστροειδοπάθεια σε Έλληνες καυκάσιους πάσχοντες από διαβήτη τύπου 2, συσχέτιση με τον πολυμορφισμό στο γονίδιο του αναστολέα του ενεργοποιητή του πλασμινογόνου 1 (ΡAI 1).” 2017. Web. 16 Apr 2021.

Vancouver:

Sokolakis T. Διαβητική αμφιβληστροειδοπάθεια σε Έλληνες καυκάσιους πάσχοντες από διαβήτη τύπου 2, συσχέτιση με τον πολυμορφισμό στο γονίδιο του αναστολέα του ενεργοποιητή του πλασμινογόνου 1 (ΡAI 1). [Internet] [Thesis]. University of Thessaly (UTH); Πανεπιστήμιο Θεσσαλίας; 2017. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/10442/hedi/42107.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Sokolakis T. Διαβητική αμφιβληστροειδοπάθεια σε Έλληνες καυκάσιους πάσχοντες από διαβήτη τύπου 2, συσχέτιση με τον πολυμορφισμό στο γονίδιο του αναστολέα του ενεργοποιητή του πλασμινογόνου 1 (ΡAI 1). [Thesis]. University of Thessaly (UTH); Πανεπιστήμιο Θεσσαλίας; 2017. Available from: http://hdl.handle.net/10442/hedi/42107

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Universiteit Utrecht

12. Kortlever, R.M. Escaping growth arrest in cancer.

Degree: 2008, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/27795

► We now have a general idea of which genes and cellular pathways are central in cancer development: uncontrolled growth governs establishment and spread of the… (more)

▼ We now have a general idea of which genes and cellular pathways are central in cancer development: uncontrolled growth governs establishment and spread of the disease. Nevertheless, to fully appreciate the consequences of the interplay of driver mutations in this genetic disease it is imperative we understand the mechanisms behind uncontrolled growth, or escape of growth arrest, in cancer. It is still not fully understood how cells escape the tumor-suppressing activity of p53, the most mutated gene in cancer. How p53 is regulated and recruited to protect against tumor formation is well known, but it is less well known how it executes this function. By studying the tumor-suppressive activity of p53 in both a biased and unbiased manner I have identified various molecules and mechanisms that may intersect with p53 function when it comes to uncontrolled cell growth, or tumor initiation. I have found that there is a reciprocal regulation of p53 and growth stimulatory signals, since activation of p53 results in an arrest in the cell cycle, or senescence, by blocking growth signaling, and that hyperactive growth factor signaling can override p53 function. Interestingly, plasminogen activator inhibitor-1 (PAI-1), one of the molecules I found to be causally involved in senescence, and which normally is activated by p53 under stressful conditions, is a secreted protein and has its most direct function on the outside of a cell. Hence, it can be regarded a gatekeeper of cell cycle progression. My findings also suggest that a molecule that formerly was coupled to extra-cellular cross-talk between cells and wound-healing apparently directly controls cycling of a cell. PAI-1 was already known to be involved in tumor progression (a process dependent on excessive communication between cells), since it highly influences metastatic behavior of a cell. For example, quantification of this molecule is used in the clinic as a marker for breast cancer progression. Next to this I screened for genes that, when hyperactivated, interfere with anti-tumorigenic p53 activity, and found that lysophosphatidic acid (LPA) activity induce a senescence-bypass. LPA is a lipid involved in growth and wound healing processes. This further supports the notion that growth factor- and p53 signaling are linked. I also found that TGFbeta, a molecule with strong tumor suppressive activity, needs PAI-1 for its anti-tumorigenic effect. One of the biggest questions regarding TGFbeta dependent tumorigenesis is what mutations drive the transition from tumor intitiation to tumor progression or, in other words, what mutations make cells less sensitive to innate anti-tumorigenic activity of stress signals. I hypothesize that PAI-1 may be a central player and necessary downstream of both anti-tumorigenic p53- and TGFbeta signaling. My findings shed light on how intra-cellular tumor-suppressive gene programs result in specific communicative behavior of cells, and support the notion that wound healing and tumor-progression have parallel mechanisms. Furthermore, it provides…

Subjects/Keywords: Geneeskunde; cancer; cell cycle; senescence; p53; plasminogen activator inhibitor-1; TGFbeta; tumor microenvironment; growth signaling; cytostasis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kortlever, R. M. (2008). Escaping growth arrest in cancer. (Doctoral Dissertation). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/27795

Chicago Manual of Style (16^th Edition):

Kortlever, R M. “Escaping growth arrest in cancer.” 2008. Doctoral Dissertation, Universiteit Utrecht. Accessed April 16, 2021. http://dspace.library.uu.nl:8080/handle/1874/27795.

MLA Handbook (7^th Edition):

Kortlever, R M. “Escaping growth arrest in cancer.” 2008. Web. 16 Apr 2021.

Vancouver:

Kortlever RM. Escaping growth arrest in cancer. [Internet] [Doctoral dissertation]. Universiteit Utrecht; 2008. [cited 2021 Apr 16]. Available from: http://dspace.library.uu.nl:8080/handle/1874/27795.

Council of Science Editors:

Kortlever RM. Escaping growth arrest in cancer. [Doctoral Dissertation]. Universiteit Utrecht; 2008. Available from: http://dspace.library.uu.nl:8080/handle/1874/27795

University of Western Ontario

13. Swarbreck, Scott. Effect of Ascorbate on Coagulation and Fibrinolytic Factors in the Septic Microvasculature.

Degree: 2014, University of Western Ontario

URL: https://ir.lib.uwo.ca/etd/2021

► Sepsis, a systemic inflammatory response to an infection, is a significant cause of morbidity and mortality worldwide. The microcirculation during sepsis fails, in part, due… (more)

▼ Sepsis, a systemic inflammatory response to an infection, is a significant cause of morbidity and mortality worldwide. The microcirculation during sepsis fails, in part, due to microthrombosis and the resulting plugging of capillaries, precipitating organ failure. Intravenous injection of ascorbate has been shown to reduce capillary plugging, however the mechanism of this protective effect is unclear. We hypothesized that ascorbate-mediated destabilization of the microthrombi through promoting fibrinolysis could contribute to this protection. We showed that streptokinase, a pro-fibrinolytic agent, reduced the capillary plugging to a similar degree as ascorbate. This similarity provided the impetus for studying the effect of ascorbate on fibrinolysis. Sepsis increased the urokinase plasminogen activator (u-PA) and tissue plasminogen activator (t-PA) mRNA expression in the skeletal muscle and liver in mice. No effect of ascorbate was observed on u-PA or t-PA expression levels. Sepsis also increased the plasminogen activator inhibitor 1 (PAI-1) mRNA and protein expression and activity in these tissues, but ascorbate did not affect these increases. The local PAI-1 release by both platelets and endothelial cells may play a critical role in microthrombus formation in capillaries. We observed that PAI-1 released by isolated endothelial cells was not affected by ascorbate. However, thrombin-induced PAI-1 release from platelets was inhibited by ascorbate pH-dependently. We have also discovered that the PAI-1 release from platelets was nitric oxide independent. It has been shown that PAI-1 has a protective role in sepsis, namely that PAI-1 knockout leads to increased bacterial content, increased neutrophil apoptosis and increased mortality. Therefore, the lack of effect of ascorbate on PAI-1 in the tissue may maintain PAI-1’s beneficial role in sepsis. Consistently, we observed that sepsis-induced increases in bacterial count, PAI-1 expression and myeloperoxidase content in various organs were not affected by ascorbate. Overall, the lack of effect of ascorbate indicates that the protection by ascorbate through reduced capillary plugging is not through a fibrinolytic mechanism. Other mechanisms such as platelet-endothelial cell adhesion and changes in red blood cell deformability in the capillaries should be explored as possible mechanisms of protection by ascorbate.

Subjects/Keywords: Sepsis; ascorbate; capillary blood flow; plasminogen activator inhibitor-1; fibrinolysis; Alternative and Complementary Medicine; Animal Diseases; Bacterial Infections and Mycoses; Pharmacology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Swarbreck, S. (2014). Effect of Ascorbate on Coagulation and Fibrinolytic Factors in the Septic Microvasculature. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/2021

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Swarbreck, Scott. “Effect of Ascorbate on Coagulation and Fibrinolytic Factors in the Septic Microvasculature.” 2014. Thesis, University of Western Ontario. Accessed April 16, 2021. https://ir.lib.uwo.ca/etd/2021.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Swarbreck, Scott. “Effect of Ascorbate on Coagulation and Fibrinolytic Factors in the Septic Microvasculature.” 2014. Web. 16 Apr 2021.

Vancouver:

Swarbreck S. Effect of Ascorbate on Coagulation and Fibrinolytic Factors in the Septic Microvasculature. [Internet] [Thesis]. University of Western Ontario; 2014. [cited 2021 Apr 16]. Available from: https://ir.lib.uwo.ca/etd/2021.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Swarbreck S. Effect of Ascorbate on Coagulation and Fibrinolytic Factors in the Septic Microvasculature. [Thesis]. University of Western Ontario; 2014. Available from: https://ir.lib.uwo.ca/etd/2021

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

14. Wilson, Shelly. MOLECULAR INSIGHTS AND PHYSIOLOGICAL CONSEQUENCES OF ARYL HYDROCARBON RECEPTOR REGULATED PLASMINOGEN ACTIVATOR INHIBITOR-1 EXPRESSION.

Degree: Doctoral, Cell Biology, 2013, The University of Texas Medical Branch at Galveston

URL: http://hdl.handle.net/2152.3/539

► The aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor, attenuates liver regeneration in vivo when activated by its prototypical agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) following 70% partial… (more)

▼ The aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor, attenuates liver regeneration in vivo when activated by its prototypical agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) following 70% partial hepatectomy (PH). One reported target of the AhR that may account for suppression of the regenerative response is plasminogen activator inhibitor-1 (PAI-1), which negatively regulates the cleavage and activation of hepatocyte growth factor (HGF) from its latent form in the extracellular matrix. Once activated, HGF signalling through its receptor cMet is a crucial component early in regeneration. Recent studies identified a sequence distinct from the canonical AhR binding site, the ncXRE, which confers TCDD-inducible expression to the PAI-1 promoter. Since the ncXRE shares partial sequence homology with the Kruppel-like factor 6 (KLF6) consensus binding site; I hypothesize that the AhR interacts with KLF6 at the ncXRE, inducing transcription of PAI-1, suppressing HGF processing and its activation of cMet, inhibiting liver regeneration. To test this hypothesis, coimmunoprecipitation on liver nuclear extracts and recombinant proteins confirmed that KLF6 and the AhR interact, likely dependent on the C-terminus transactivating domain of AhR and the DNA binding domain of KLF6. Both proteins bind the ncXRE in vitro and deletion analyses revealed that the N-terminal 27 amino acids of hKLF6 were required for complex formation. Chromatin immunoprecipitation studies demonstrated that the AhR and KLF6 bind to the PAI-1 promoter in vivo. To assess the effects of AhR activation in vivo, C57BL/6 and PAI-1-/- mice were pretreated with TCDD, underwent PH, and liver samples and serum were collected at multiple time points post-PH to monitor PAI-1 expression, HGF processing, and cMet phosphorylation (activation) and DNA synthesis in the liver. I found that PAI-1 transcript and corresponding serum PAI-1 protein levels were markedly increased in TCDD-pretreated C57BL/6 mice, and this rise in PAI-1 levels inversely correlated to HGF processing and cMet phosphorylation. Hepatocytes in the periportal region of PAI-1-/- mice were able to overcome TCDD-mediated suppression of regeneration. The AhR-KLF6 interaction at the PAI-1 promoter, resulting in increased PAI-1 expression and decreased HGF processing and cMet activation, reveals a novel mechanism by which the AhR may contribute to liver homeostasis. Advisors/Committee Members: Elferink, Cornelis (advisor), Barton, Michelle (committee member), Cicalese, Luca (committee member), Boor, Paul (committee member), Papaconstantinou, John (committee member).

Subjects/Keywords: aryl hydrocarbon receptor; kruppel-like factor 6; plasminogen activator inhibitor-1; liver regeneration; hepatocyte growth factor; cMet; TCDD; dioxin

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Wilson, S. (2013). MOLECULAR INSIGHTS AND PHYSIOLOGICAL CONSEQUENCES OF ARYL HYDROCARBON RECEPTOR REGULATED PLASMINOGEN ACTIVATOR INHIBITOR-1 EXPRESSION. (Doctoral Dissertation). The University of Texas Medical Branch at Galveston. Retrieved from http://hdl.handle.net/2152.3/539

Chicago Manual of Style (16^th Edition):

Wilson, Shelly. “MOLECULAR INSIGHTS AND PHYSIOLOGICAL CONSEQUENCES OF ARYL HYDROCARBON RECEPTOR REGULATED PLASMINOGEN ACTIVATOR INHIBITOR-1 EXPRESSION.” 2013. Doctoral Dissertation, The University of Texas Medical Branch at Galveston. Accessed April 16, 2021. http://hdl.handle.net/2152.3/539.

MLA Handbook (7^th Edition):

Wilson, Shelly. “MOLECULAR INSIGHTS AND PHYSIOLOGICAL CONSEQUENCES OF ARYL HYDROCARBON RECEPTOR REGULATED PLASMINOGEN ACTIVATOR INHIBITOR-1 EXPRESSION.” 2013. Web. 16 Apr 2021.

Vancouver:

Wilson S. MOLECULAR INSIGHTS AND PHYSIOLOGICAL CONSEQUENCES OF ARYL HYDROCARBON RECEPTOR REGULATED PLASMINOGEN ACTIVATOR INHIBITOR-1 EXPRESSION. [Internet] [Doctoral dissertation]. The University of Texas Medical Branch at Galveston; 2013. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/2152.3/539.

Council of Science Editors:

Wilson S. MOLECULAR INSIGHTS AND PHYSIOLOGICAL CONSEQUENCES OF ARYL HYDROCARBON RECEPTOR REGULATED PLASMINOGEN ACTIVATOR INHIBITOR-1 EXPRESSION. [Doctoral Dissertation]. The University of Texas Medical Branch at Galveston; 2013. Available from: http://hdl.handle.net/2152.3/539

Queens University

15. Cook, P. Michael. A Quantitative Investigation of Selected Reactions in the Fibrinolytic Cascade .

Degree: Biochemistry, 2008, Queens University

URL: http://hdl.handle.net/1974/1014

► Previous work has shown that thrombin activatable fibrinolysis inhibitor (TAFI) was unable to prolong lysis of purified clots in the presence of Lys-plasminogen (Lys-Pg), indicating… (more)

▼ Previous work has shown that thrombin activatable fibrinolysis inhibitor (TAFI) was unable to prolong lysis of purified clots in the presence of Lys-plasminogen (Lys-Pg), indicating a possible mechanism for fibrinolysis to circumvent prolongation mediated by activated TAFI (TAFIa). Therefore, the effects of TAFIa on Lys-Pg activation and Lys-plasmin (Lys-Pn) inhibition by antiplasmin (AP) were quantitatively investigated using a fluorescently labeled recombinant Pg mutant which does not produce active Pn. High molecular weight fibrin degradation products (HMW-FDPs), a soluble fibrin surrogate that models Pn modified fibrin, treated with TAFIa decreased the catalytic efficiency (kcat/Km) of 5IAF-Glu-Pg cleavage by 417-fold and of 5IAF-Lys-Pg cleavage by 55-fold. A previously devised intact clot system was used to measure the apparent second order rate constant (k2) for Pn inhibition by AP over time. While TAFIa was able to abolish the protection associated with Pn modified fibrin in clots formed with Glu-Pg, it was not able to abolish the protection in clots formed with Lys-Pg. However, TAFIa was still able to prolong the lysis of clots formed with Lys-Pg. TAFIa prolongs clot lysis by removing the positive feedback loop for Pn generation. The effect of TAFIa modification of the HMW-FDPs on the rate of tissue type plasminogen activator (tPA) inhibition by plasminogen activator inhibitor type 1 (PAI-1) was investigated using a previously devised end point assay. HMW-FDPs decreased the k2 for tPA inhibition rate by 3-fold. Thus, HMW-FDPs protect tPA from PAI-1. TAFIa treatment of the HMW-FDPs resulted in no change in protection. Vitronectin also did not appreciably affect tPA inhibition by PAI-1. Pg, in conjunction with HMW-FDPs, decreased the k2 for tPA inhibition by 30-fold. Hence, Pg, when bound to HMW-FDPs, protects tPA by an additional 10-fold. TAFIa treatment of the HMW-FDPs completely removed this additional protection provided by Pg. In conclusion, an additional mechanism was identified whereby TAFIa can prolong clot lysis by increasing the rate of tPA inhibition by PAI-1 by eliminating the protective effects of Pn-modified fibrin and Pg. Because TAFIa can suppress Lys-Pg activation but cannot attenuate Lys-Pn inhibition by AP, the Glu- to Lys-Pg/Pn conversion is able to act as a fibrinolytic switch to ultimately lyse the clot.

Subjects/Keywords: Thrombin Activatable Fibrinolysis Inhibitor ; Procarboxypeptidase U ; Fibrinolysis ; Plasminogen ; Tissue Plasminogen Activator ; Plasminogen Activator Inhibitor Type 1 ; Plasmin ; Antiplasmin ; Enzyme Kinetics ; Fibrin

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Cook, P. M. (2008). A Quantitative Investigation of Selected Reactions in the Fibrinolytic Cascade . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/1014

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Cook, P Michael. “A Quantitative Investigation of Selected Reactions in the Fibrinolytic Cascade .” 2008. Thesis, Queens University. Accessed April 16, 2021. http://hdl.handle.net/1974/1014.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Cook, P Michael. “A Quantitative Investigation of Selected Reactions in the Fibrinolytic Cascade .” 2008. Web. 16 Apr 2021.

Vancouver:

Cook PM. A Quantitative Investigation of Selected Reactions in the Fibrinolytic Cascade . [Internet] [Thesis]. Queens University; 2008. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1974/1014.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Cook PM. A Quantitative Investigation of Selected Reactions in the Fibrinolytic Cascade . [Thesis]. Queens University; 2008. Available from: http://hdl.handle.net/1974/1014

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

16. Vučković Biljana. Poremećaj funkcionalnosti fibrinoliznog mehanizma kod bolesnika sa venskom trombozom.

Degree: 2014, University of Novi Sad

URL: https://www.cris.uns.ac.rs/DownloadFileServlet/Disertacija140247280511056.pdf?controlNumber=(BISIS)87834&fileName=140247280511056.pdf&id=2206&source=OATD&language=en ; https://www.cris.uns.ac.rs/record.jsf?recordId=87834&source=OATD&language=en

► Tromboza danas, u većini razvijenih zemalja, predstavlja vodeći uzrok obolevanja i umiranja. Poslednjih godina veoma aktuelna su istraživanja venskog tromboembolizma, obzirom da je incidenca… (more)

▼ Tromboza danas, u većini razvijenih zemalja, predstavlja vodeći uzrok obolevanja i umiranja. Poslednjih godina veoma aktuelna su istraživanja venskog tromboembolizma, obzirom da je incidenca ovog oboljenja 2/1000 osoba godišnje, a njegov razvoj posledica udruženog delovanja više genetskih i stečenih faktora rizika. Što preciznije prepoznavanje i sagledavanje što većeg broja ovih faktora osnovni je cilj u borbi, kako protiv prve epizode venske tromboze, tako i protiv recidiva ove bolesti. Brojni faktori rizika već su prepoznati kao sastavne karike patofiziološkog lanca venskog trombotskog procesa, ali je evidentno da otkrića mnogih od njih tek predstoje. Među najaktulenijim istraživanjima na ovom polju nalazi se i ispitivanje uloge poremećaja fibrinoliznog mehanizma u venskoj tromboembolijskoj bolesti. Iako su već pruženi dokazi da suprimirana fibrinolizna aktivnost povećava rizik od nastanka ovog oboljenja, još uvek postoje brojna otvorena pitanja, koja se pre svega odnose na ulogu pojedinačnih činilaca fibrinoliznog mehanizma u venskoj trombozi, kao i na globalnu ulogu fibrinoliznog mehanizma u različitim tipovima i lokalizacijama venske trombotske bolesti. Pored toga, ispitivanje uticaja pojedinih genskih mutacija na pojadinačne činioce fibrinoliznog mehanizma, njegovu globalnu funkcionalnost i posredno na rizik za nastanak venske tromboze, takođe zaokuplja pažnju stručne javnosti, obzirom na nekonzistentnost rezultata dobijenih studijama koje se bave ovom problematikom. Cilj ovoga istraživanja je ispitivanje kako globalne funkcionalnosti fibrinoliznog mehanizma, tako i njegovih pojedinačnih činilaca, kod bolesnika sa različitim tipovima i lokalizacijama venske tromboze i poređenje ovih parametara sa njihovim vrednostima u zdravoj populaciji. Pored toga, cilj istraživanja je i ispitivanje zastupljenosti 4G/5G PAI-1 polimorfizma kod bolesnika sa venskom trombozom u poređenju sa zdravim osobama. Ispitivanu grupu je sačinjavalo 100 bolesnika koji su doživeli trombozu dubokih vena a kontrolnu grupu je činilo 100 zdravih ispitanika, koji nikada nisu imali trombozni incident. Iz ispitivanja su isključene: osobe sa prethodno dokazanim poremećajem hemostaznog mehanizma, osobe koje uzimaju lekove za koje se zna da mogu imati uticaja na hemostazni mehanizam, osobe koje su imale akutnu bolest u momentu uzorkovanja krvi ili 6 nedelja pre toga, osobe sa malignitetom, trudnice, osobe sa težim duševnim bolestima, bolestima jetre i bubrega, autoimunim bolestima, ispitanici koji su odbili da potpišu pristanak informisanog ispitanika. Kao test za procenu globalne funkcionalnosti fibrinoliznog mehanizma korišteno je euglobulinsko vreme lize koaguluma, dok su od pojedinačnih činilaca određivani: tkivni aktivator plazminogena (t-PA) i trombinom aktivišući fibrinolizni inhibitor (TAFI) - ELISA metodom, kao i inhibitor aktivatora plazminogena-1 (PAI-1) - metodom hromogenog substrata. Genetskim ispitivanjem je utvrđivano prisustvo PAI-1 4G/5G genskog polimorfizma.… Advisors/Committee Members: Mitić Gorana, Stošić Zoran, Đorđević Valentina, Srdanović Ilija, Popović Vladan, Đerić Mirjana.

Subjects/Keywords: Venska tromboza; Fibrinoliza; Faktori rizika; Genetski polimorfizam; Inhibitor aktivatora plazminogena 1; Venous Thrombosis; Fibrinolysis; Risk Factors; Polymorphism, Genetic; Plasminogen Activator Inhibitor 1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Biljana, V. (2014). Poremećaj funkcionalnosti fibrinoliznog mehanizma kod bolesnika sa venskom trombozom. (Thesis). University of Novi Sad. Retrieved from https://www.cris.uns.ac.rs/DownloadFileServlet/Disertacija140247280511056.pdf?controlNumber=(BISIS)87834&fileName=140247280511056.pdf&id=2206&source=OATD&language=en ; https://www.cris.uns.ac.rs/record.jsf?recordId=87834&source=OATD&language=en

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Biljana, Vučković. “Poremećaj funkcionalnosti fibrinoliznog mehanizma kod bolesnika sa venskom trombozom.” 2014. Thesis, University of Novi Sad. Accessed April 16, 2021. https://www.cris.uns.ac.rs/DownloadFileServlet/Disertacija140247280511056.pdf?controlNumber=(BISIS)87834&fileName=140247280511056.pdf&id=2206&source=OATD&language=en ; https://www.cris.uns.ac.rs/record.jsf?recordId=87834&source=OATD&language=en.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Biljana, Vučković. “Poremećaj funkcionalnosti fibrinoliznog mehanizma kod bolesnika sa venskom trombozom.” 2014. Web. 16 Apr 2021.

Vancouver:

Biljana V. Poremećaj funkcionalnosti fibrinoliznog mehanizma kod bolesnika sa venskom trombozom. [Internet] [Thesis]. University of Novi Sad; 2014. [cited 2021 Apr 16]. Available from: https://www.cris.uns.ac.rs/DownloadFileServlet/Disertacija140247280511056.pdf?controlNumber=(BISIS)87834&fileName=140247280511056.pdf&id=2206&source=OATD&language=en ; https://www.cris.uns.ac.rs/record.jsf?recordId=87834&source=OATD&language=en.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Biljana V. Poremećaj funkcionalnosti fibrinoliznog mehanizma kod bolesnika sa venskom trombozom. [Thesis]. University of Novi Sad; 2014. Available from: https://www.cris.uns.ac.rs/DownloadFileServlet/Disertacija140247280511056.pdf?controlNumber=(BISIS)87834&fileName=140247280511056.pdf&id=2206&source=OATD&language=en ; https://www.cris.uns.ac.rs/record.jsf?recordId=87834&source=OATD&language=en

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

17. Fokter Dovnik, Nina. Napovedna moč nekaterih kliničnih, histopatoloških in bioloških parametrov za preživetje bolnic z rakom dojk brez zasevkov v bezgavkah, zdravljenih v Univerzitetnem kliničnem centru Maribor v letih 2000–2009.

Degree: 2017, Univerza v Mariboru

URL: https://dk.um.si/IzpisGradiva.php?id=60104 ; https://dk.um.si/Dokument.php?id=109430&dn= ; https://plus.si.cobiss.net/opac7/bib/289117184?lang=sl

►

Izhodišča. Enega izmed največjih izzivov pri zdravljenju raka dojk v zgodnjem stadiju predstavlja izbor bolnic s predvidenim agresivnejšim potekom bolezni, ki potrebujejo dopolnilno sistemsko zdravljenje.… (more)

▼

Izhodišča. Enega izmed največjih izzivov pri zdravljenju raka dojk v zgodnjem stadiju predstavlja izbor bolnic s predvidenim agresivnejšim potekom bolezni, ki potrebujejo dopolnilno sistemsko zdravljenje. O tem se odločamo na podlagi različnih napovednih dejavnikov, kot so status pazdušnih bezgavk, velikost tumorja, stopnja diferenciacije, limfovaskularna invazija, starost bolnic, status hormonskih receptorjev, status HER2, v zadnjem času pa v ta namen ponekod uporabljajo tudi urokinazni aktivator plazminogena (uPA) in inhibitor aktivatorja plazminogena 1 (PAI-1). Vloga novejših napovednih dejavnikov v primerjavi s tradicionalnimi še ni povsem razjasnjena. Namen raziskave je bil ugotoviti vpliv posameznih dejavnikov na preživetje bolnic z rakom dojk brez zasevkov v bezgavkah, zdravljenih v Univerzitetnem kliničnem centru (UKC) Maribor. Hkrati sem želela tudi primerjati preživetje bolnic, zdravljenih v UKC Maribor, s slovenskim povprečjem. Bolnice in metode. Opravila sem retrospektivno analizo bolnic z invazivnim rakom dojk brez zasevkov v bezgavkah, ki so bile primarno zdravljene v UKC Maribor v letih 2000–2009. Podatke sem pridobila iz medicinske dokumentacije in jih dopolnila s podatki iz Registra raka Republike Slovenije, od koder sem pridobila tudi podatke o vseh primerljivih slovenskih bolnicah, zdravljenih v istem obdobju. Analizirala sem korelacije med napovednimi dejavniki in s pomočjo Coxove regresije in Coxovega modela sorazmernih tveganj opravila univariatne in multivariatne analize preživetja brez bolezni, celokupnega in specifičnega preživetja. Rezultati. Študijsko skupino je sestavljalo 858 bolnic s srednjim časom sledenja 101 mesec. Med bolnicami, zdravljenimi v UKC Maribor, in vsemi slovenskimi bolnicami ni bilo razlik v celokupnem (HR 1,07

95 % CI 0,91–1,27

p = 0,413) in specifičnem preživetju (HR 0,85

95 % CI 0,66–1,11

p = 0,234). Preživetje brez bolezni (HR 0,67

95 % CI 0,50–0,91

p = 0,010) in specifično preživetje (HR 0,53

95 % CI 0,30–0,94

p = 0,031) je bilo statistično značilno boljše v obdobju 2005–2009 v primerjavi z 2000–2004, pri celokupnem preživetju pa se je kazal enako usmerjen statistično neznačilen trend (HR 0,73

95 % CI 0,51–1,05

p = 0,087). Med napovednimi dejavniki so bile prisotne številne korelacije. V multivariatnih analizah so na preživetje brez bolezni najbolj vplivali starost ob diagnozi, vrednost uPA/PAI-1 in status estrogenskih receptorjev, na celokupno preživetje starost, stopnja diferenciacije in vrednost uPA/PAI-1, na specifično preživetje pa stopnja diferenciacije. Zaključki. Preživetje bolnic z rakom dojk brez zasevkov v bezgavkah, primarno zdravljenih v UKC Maribor v letih 2000–2009, je zelo visoko in enakovredno preživetju vseh primerljivih bolnic na ravni Slovenije. Kot najpomembnejša napovedna dejavnika sta se pri tej skupini bolnic izkazala vrednost uPA/PAI-1 in stopnja diferenciacije, ki sta klinično pomembno vplivala na preživetje brez bolezni, celokupno in specifično preživetje.

Introduction. The choice of patients with an…

Advisors/Committee Members: Takač, Iztok.

Subjects/Keywords: rak dojk brez zasevkov v bezgavkah; dopolnilno zdravljenje; stadij; stopnja diferenciacije; status HER2; status hormonskih receptorjev; urokinazni aktivator plazminogena; inhibitor aktivatorja plazminogena 1; node negative breast cancer; adjuvant treatment; stage; tumour grade; HER2 status; hormone receptor status; urokinase plasminogen activator; plasminogen activator inhibitor 1

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❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Fokter Dovnik, N. (2017). Napovedna moč nekaterih kliničnih, histopatoloških in bioloških parametrov za preživetje bolnic z rakom dojk brez zasevkov v bezgavkah, zdravljenih v Univerzitetnem kliničnem centru Maribor v letih 2000–2009. (Doctoral Dissertation). Univerza v Mariboru. Retrieved from https://dk.um.si/IzpisGradiva.php?id=60104 ; https://dk.um.si/Dokument.php?id=109430&dn= ; https://plus.si.cobiss.net/opac7/bib/289117184?lang=sl

Chicago Manual of Style (16^th Edition):

Fokter Dovnik, Nina. “Napovedna moč nekaterih kliničnih, histopatoloških in bioloških parametrov za preživetje bolnic z rakom dojk brez zasevkov v bezgavkah, zdravljenih v Univerzitetnem kliničnem centru Maribor v letih 2000–2009.” 2017. Doctoral Dissertation, Univerza v Mariboru. Accessed April 16, 2021. https://dk.um.si/IzpisGradiva.php?id=60104 ; https://dk.um.si/Dokument.php?id=109430&dn= ; https://plus.si.cobiss.net/opac7/bib/289117184?lang=sl.

MLA Handbook (7^th Edition):

Fokter Dovnik, Nina. “Napovedna moč nekaterih kliničnih, histopatoloških in bioloških parametrov za preživetje bolnic z rakom dojk brez zasevkov v bezgavkah, zdravljenih v Univerzitetnem kliničnem centru Maribor v letih 2000–2009.” 2017. Web. 16 Apr 2021.

Vancouver:

Fokter Dovnik N. Napovedna moč nekaterih kliničnih, histopatoloških in bioloških parametrov za preživetje bolnic z rakom dojk brez zasevkov v bezgavkah, zdravljenih v Univerzitetnem kliničnem centru Maribor v letih 2000–2009. [Internet] [Doctoral dissertation]. Univerza v Mariboru; 2017. [cited 2021 Apr 16]. Available from: https://dk.um.si/IzpisGradiva.php?id=60104 ; https://dk.um.si/Dokument.php?id=109430&dn= ; https://plus.si.cobiss.net/opac7/bib/289117184?lang=sl.

Council of Science Editors:

Fokter Dovnik N. Napovedna moč nekaterih kliničnih, histopatoloških in bioloških parametrov za preživetje bolnic z rakom dojk brez zasevkov v bezgavkah, zdravljenih v Univerzitetnem kliničnem centru Maribor v letih 2000–2009. [Doctoral Dissertation]. Univerza v Mariboru; 2017. Available from: https://dk.um.si/IzpisGradiva.php?id=60104 ; https://dk.um.si/Dokument.php?id=109430&dn= ; https://plus.si.cobiss.net/opac7/bib/289117184?lang=sl

18. OLIVEIRA, Georgge Gomes. Polimorfismo da região -675 do gene serpine1 (polimorfismo 4g5g) e sua associação com inibidor 1 da ativação do plasminogenio (pai-1), síndrome metabólica e risco cardiovascular em pessoas vivendo com hiv/aids: um estudo caso-controle aninhado à coorte.

Degree: 2015, Federal University of Pernambuco

URL: https://repositorio.ufpe.br/handle/123456789/18083

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Ministério da Saúde do Brasil

Estudos recentes mostram que a síndrome metabólica (SM) é freqüente nas pessoas vivendo com HIV/AIDS (PLWHA). A importância na identificação… (more)

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Ministério da Saúde do Brasil

Estudos recentes mostram que a síndrome metabólica (SM) é freqüente nas pessoas vivendo com HIV/AIDS (PLWHA). A importância na identificação da SM baseia-se no aumento do risco em cinco vezes de desenvolver diabetes mellitus tipo 2 (DM2) e em duas vezes de apresentar doença cardiovascular (DCV) trombóticas, embora os fatores de hipercoagulabilidade não estejam incluídos nos critérios de definição da síndrome. A SM é caracterizada pela presença concomitante de fatores reconhecidamente aterogênicos em um mesmo indivíduo. A freqüência de DCV em PLWHA vem aumentando ao longo dos anos. O PAI-1 é uma proteína importante na cascata de fibrinólise e seu aumento está associado ao estado de hipercoagulabilidade. Sua regulação depende de fatores genéticos, dentre eles, destaca-se o polimorfismo 4G5G do gene SERPINE1. A participação de substâncias protrombóticas na doença cardiovascular é conhecida em pessoas sem HIV, porém menos elucidada em PLWHA. Diante disto o objetivo deste trabalho foi determinar a freqüência do polimorfismo 4G5G em pessoas que vivem com HIV e verificar se o polimorfismo tem associação com a expressão do PAI-1 plasmático, com SM e com risco cardiovascular (RCV) estimado pelo escore de Framingham. Também objetivamos verificar associação dos níveis de PAI-1 com RDC e com SM. Para tanto foi desenvolvido estudo transversal para determinação da freqüência do polimorfismo 4G5G do PAI-1 e estudo tipo caso-controle para verificar associações entre polimorfismos com níveis plasmáticos de PAI-1 com SM e depois com RCV. Também foram testadas associações com fatores de risco tradicionais. Para primeiro estudo a amostra foi 185 pessoas sorteadas de um grupo de 2074 participantes da Cohort AIDS-PE Study Group. A prevalência de heterozigose foi de 86,8% e homozigose para 4G4G de 4,4%. A média de idade foi de 40,5 (DP ± 9,9 anos). A mediana de PAI-1 ativado foi de 13,6 ng/mL (IQ: 10,8-17,5). A freqüência de SM foi de 37,9% e de dislipidemia de 82,4%. Não encontramos associação do polimorfismo com os níveis plasmáticos de PAI-1, nem com SM. Para o segundo estudo houve perda de 23, restando 162 pessoas das quais 72,8% era do sexo feminino e a média de idade foi de 40 anos. A freqüência de RDCV estimado > 10% foi de 10,5%. O alelo 4G esteve presente em 91,0% das pessoas (genótipos 4G4G e 4G5G). Não houve associação entre polimorfismo e RDCV estimado > 10% (OR=0,6; IC95% 0,1 – 3,7), nem diferença dos níveis de PAI-1 em relação ao RDCV estimado (RCV>10% 14,6 ng/ml x RDCV < 10% 14,1 ng/ml; ρ=0,9). Hipercolesterolemia foi associada com genótipo 5G5G do polimorfismo (OR: 3,3; IC95%: 1,25 – 10) e com níveis plasmáticos mais elevados do PAI-1 (colesterol não HDL (CNHDL) > 130 mg/dl = 15,6 ng/ml versus CNHDL < 130 ng/ml = 13,8 ng/ml; ρ=0,04). Nesse estudo, encontramos alta prevalência do heterozigose para o polimorfismo 4G5G em pessoas vivendo com HIV/AIDS, no nordeste do Brasil. Entretanto, não encontramos associação entre o polimorfismo estudado com níveis plasmáticos de PAI-1 nem com SM. Também…

Advisors/Committee Members: http://buscatextual.cnpq.br/buscatextual/busca.do, XIMENES, Ricardo Arraes de Alencar.

Subjects/Keywords: Inibidor 1 de ativador de plasminogênio (PAI-1) ▪ Polimorfismo Genético ▪ Síndrome X metabólica ▪ HIV ▪ Framingham; Plasminogen Activator Inhibitor 1 (PAI-1 ) ▪ Polymorphism, Genetic ▪ Metabolic syndrome X ▪ HIV ▪ Framingham .

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

OLIVEIRA, G. G. (2015). Polimorfismo da região -675 do gene serpine1 (polimorfismo 4g5g) e sua associação com inibidor 1 da ativação do plasminogenio (pai-1), síndrome metabólica e risco cardiovascular em pessoas vivendo com hiv/aids: um estudo caso-controle aninhado à coorte. (Doctoral Dissertation). Federal University of Pernambuco. Retrieved from https://repositorio.ufpe.br/handle/123456789/18083

Chicago Manual of Style (16^th Edition):

OLIVEIRA, Georgge Gomes. “Polimorfismo da região -675 do gene serpine1 (polimorfismo 4g5g) e sua associação com inibidor 1 da ativação do plasminogenio (pai-1), síndrome metabólica e risco cardiovascular em pessoas vivendo com hiv/aids: um estudo caso-controle aninhado à coorte.” 2015. Doctoral Dissertation, Federal University of Pernambuco. Accessed April 16, 2021. https://repositorio.ufpe.br/handle/123456789/18083.

MLA Handbook (7^th Edition):

OLIVEIRA, Georgge Gomes. “Polimorfismo da região -675 do gene serpine1 (polimorfismo 4g5g) e sua associação com inibidor 1 da ativação do plasminogenio (pai-1), síndrome metabólica e risco cardiovascular em pessoas vivendo com hiv/aids: um estudo caso-controle aninhado à coorte.” 2015. Web. 16 Apr 2021.

Vancouver:

OLIVEIRA GG. Polimorfismo da região -675 do gene serpine1 (polimorfismo 4g5g) e sua associação com inibidor 1 da ativação do plasminogenio (pai-1), síndrome metabólica e risco cardiovascular em pessoas vivendo com hiv/aids: um estudo caso-controle aninhado à coorte. [Internet] [Doctoral dissertation]. Federal University of Pernambuco; 2015. [cited 2021 Apr 16]. Available from: https://repositorio.ufpe.br/handle/123456789/18083.

Council of Science Editors:

OLIVEIRA GG. Polimorfismo da região -675 do gene serpine1 (polimorfismo 4g5g) e sua associação com inibidor 1 da ativação do plasminogenio (pai-1), síndrome metabólica e risco cardiovascular em pessoas vivendo com hiv/aids: um estudo caso-controle aninhado à coorte. [Doctoral Dissertation]. Federal University of Pernambuco; 2015. Available from: https://repositorio.ufpe.br/handle/123456789/18083

University of Wollongong

19. Lee, Jodi Anne. Characterisation of SerpinB2 as a stress response modulator.

Degree: PhD, 2015, University of Wollongong

URL: ; https://ro.uow.edu.au/theses/4538

► SerpinB2 [plasminogen activator inhibitor type-2 (PAI-2)] was first described as a placental protein, which regulated plasminogen activation via the inhibition of the urokinase (uPA)… (more)

Subjects/Keywords: Serpin82; PAI-2; plasminogen activator inhibitor type-2; stress response; chaperone; tissue plasmin·ogen activator; urokinase plasminogen activator; proteostasis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lee, J. A. (2015). Characterisation of SerpinB2 as a stress response modulator. (Doctoral Dissertation). University of Wollongong. Retrieved from ; https://ro.uow.edu.au/theses/4538

Chicago Manual of Style (16^th Edition):

Lee, Jodi Anne. “Characterisation of SerpinB2 as a stress response modulator.” 2015. Doctoral Dissertation, University of Wollongong. Accessed April 16, 2021. ; https://ro.uow.edu.au/theses/4538.

MLA Handbook (7^th Edition):

Lee, Jodi Anne. “Characterisation of SerpinB2 as a stress response modulator.” 2015. Web. 16 Apr 2021.

Vancouver:

Lee JA. Characterisation of SerpinB2 as a stress response modulator. [Internet] [Doctoral dissertation]. University of Wollongong; 2015. [cited 2021 Apr 16]. Available from: ; https://ro.uow.edu.au/theses/4538.

Council of Science Editors:

Lee JA. Characterisation of SerpinB2 as a stress response modulator. [Doctoral Dissertation]. University of Wollongong; 2015. Available from: ; https://ro.uow.edu.au/theses/4538

Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ)

20. Karabouta, Zacharoula. Διερεύνηση του πολυμορφισμού του γονιδίου του αναστολέα του ενεργοποιητή του πλασμινογόνου-1 και των επιπέδων του στον ορό, σε παιδιά και εφήβους με αυξημένο δείκτη μάζας σώματος.

Degree: 2018, Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ)

URL: http://hdl.handle.net/10442/hedi/43438

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Introduction. PAI-1 is the main inhibitor of plasminogen activators and thus of fibrinolysis. Increased PAI-1 plasma levels are found in various conditions, like obesity, dyslipidaemia,… (more)

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Introduction. PAI-1 is the main inhibitor of plasminogen activators and thus of fibrinolysis. Increased PAI-1 plasma levels are found in various conditions, like obesity, dyslipidaemia, insulin resistance (IR), cardiovascular disease (CVD) and cancer. PAI-1 has been associated with increased atherothrombosis in those conditions. Studies have shown a correlation between plasma PAI-1 levels and the polymorphism 4G/5G 4G(rs1799762) of the promoter of the PAI-1 gene.Aim. The aim of the study was to investigate the correlation between polymorphism 4G/5G(rs1799762) and plasma PAI-1 levels in overweight/obese children and adolescents and compare them with controls of normal body mass index (BMI).Subjects and methods. 99 obese/overweight children/adolescents (mean age 9.9 (± 2.8 years) and 93 healthy controls (mean age 10 ± 2.1 years) were included in the study. Anthropometric studies were performed, serum PAI-1 levels and fasting biochemical indices (TC, HDL-C, LDL-C, Tg, Apo(A), Apo(B), Lp(a), glucose(FBG), insulin(FI), SGOT (AST), SGPT (ALT), γGT, uric acid, hsCRP), were measured. Genotypes 4G/4G, 4G/5G and 5G/5G of the 4G/5G polymorphism were studied from the isolation of DNA from whole blood with RT-PCR and High Resolution Method (HRM). Statistical analysis was performed with IBM Statistics SPSS 20.0, statistical significance was set for p<0.05.Results. The mean values of TC, Tg, Apo(B), FI, HOMA-IR, SGPT (ALT), γ-GT, uric acid, hsCRP, plasma PAI-1 levels, were found statistically significantly higher in the overweight/obese group when compared to the corresponding values of the control group, HDL-C and Apo(A) were significantly lower. No statistically significant difference was observed for variables LDL-C, Lp(a), FBG, SGOT (AST). A tendency was shown for Lp(a) to be increased in the overweight/obese children and adolescents compared to the controls. Mean plasma PAI-1 levels in the prepubertal overweight/obese group were statistically significantly higher compared to the prepubertal control group. Only for the 4G/4G and 5G/5G genotypes statistically, a significant difference was observed between overweight/obese and controls. 4G/4G genotype was found in a higher percentage in the overweight/obese, 5G/5G in the controls. No statistically significant difference was found for the 4G/5G genotype. Plasma PAI-1 mean value was statistically significantly higher only in the overweight/obese 4G/4G and 5G/5G group compared to the controls corresponding ones, no statistically significant difference was observed between 4G/4G and 5G/5G overweight/obese and between 4G/4G και 5G/5G controls. Conclusion. Overweight/obese children/adolescents had elevated plasma PAI-1 levels and significantly commoner 4G/4G genotype compared to controls where the 5G/5G genotype was commoner. No difference was found for the 4G/5G genotype between the two groups. The 4G allele maybe is a significant risk factor for the development of CVD in adulthood. However, more studies are required to draw a final conclusion.

Εισαγωγή. Ο ΡΑΙ-1 είναι ο κύριος…

Subjects/Keywords: Παιδιά και έφηβοι; Υπερβαρότητα και παχυσαρκία; Αναστολέας του ενεργοποιητή του πλασμινογόνου-1; Πολυμορφισμός 4G/5G; Children and adolescents; Overweight and obesity; Plasminogen activator inhibitor-1 (PAI-1); 4G/5G polymorphism

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Karabouta, Z. (2018). Διερεύνηση του πολυμορφισμού του γονιδίου του αναστολέα του ενεργοποιητή του πλασμινογόνου-1 και των επιπέδων του στον ορό, σε παιδιά και εφήβους με αυξημένο δείκτη μάζας σώματος. (Thesis). Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ). Retrieved from http://hdl.handle.net/10442/hedi/43438

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Karabouta, Zacharoula. “Διερεύνηση του πολυμορφισμού του γονιδίου του αναστολέα του ενεργοποιητή του πλασμινογόνου-1 και των επιπέδων του στον ορό, σε παιδιά και εφήβους με αυξημένο δείκτη μάζας σώματος.” 2018. Thesis, Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ). Accessed April 16, 2021. http://hdl.handle.net/10442/hedi/43438.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Karabouta, Zacharoula. “Διερεύνηση του πολυμορφισμού του γονιδίου του αναστολέα του ενεργοποιητή του πλασμινογόνου-1 και των επιπέδων του στον ορό, σε παιδιά και εφήβους με αυξημένο δείκτη μάζας σώματος.” 2018. Web. 16 Apr 2021.

Vancouver:

Karabouta Z. Διερεύνηση του πολυμορφισμού του γονιδίου του αναστολέα του ενεργοποιητή του πλασμινογόνου-1 και των επιπέδων του στον ορό, σε παιδιά και εφήβους με αυξημένο δείκτη μάζας σώματος. [Internet] [Thesis]. Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ); 2018. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/10442/hedi/43438.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Karabouta Z. Διερεύνηση του πολυμορφισμού του γονιδίου του αναστολέα του ενεργοποιητή του πλασμινογόνου-1 και των επιπέδων του στον ορό, σε παιδιά και εφήβους με αυξημένο δείκτη μάζας σώματος. [Thesis]. Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ); 2018. Available from: http://hdl.handle.net/10442/hedi/43438

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Gothenburg / Göteborgs Universitet

21. Hultman, Karin. On the Regulation of the Serine Protease t-PA and its Inhibitor PAI-1 in the Brain.

Degree: 2010, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/22903

► The serine protease tissue-type plasminogen activator (t-PA) is the main fibrinolytic enzyme in the vascular system, and thus plays a critical role in the dissolution… (more)

▼ The serine protease tissue-type plasminogen activator (t-PA) is the main fibrinolytic enzyme in the vascular system, and thus plays a critical role in the dissolution of thrombi. In recent years, researchers have focused on its role within the brain, where t-PA has been shown to participate in a number of physiological and pathophysiological processes, including various aspects of synaptic plasticity and neurodegeneration. To date, knowledge on how t-PA and its inhibitors are regulated in the brain has mainly been gained from murine in vitro and in vivo models. However, in view of the species-specific differences in the expression of these genes, the question remains as to how well the results obtained in animal models can be extrapolated to humans. Therefore, the work described in this thesis was directed at improving our knowledge on the regulation of t-PA and its principal inhibitor plasminogen activator inhibitor type-1 (PAI-1) in the human brain. In this thesis, it is described for the first time that astrocytes have an intracellular storage compartment for t-PA, the levels of which can be increased in response to retinoic acid and protein kinase C activation. Regulated release of t-PA is induced in response to forskolin and histamine, which implies that astrocytes contribute to the extracellular levels of t-PA within the human brain. Expression studies of PAI-1 and of another t-PA inhibitor, protease nexin-1 (PN-1), revealed that the astrocytic expression levels of these inhibitors are regulated in a dynamic manner by injury-related factors, such as cytokines and hypoxia. This response may represent an important protective mechanism to reduce neurotoxicity under conditions of excessive t-PA activity, such as in the acute phase of cerebral ischaemia and in epilepsy. Given the compelling evidence that excessive t-PA activity results in the breakdown of the blood-brain barrier (BBB), the expression profiles of t-PA, PAI-1 and PN-1 were also investigated in a rodent in vitro model of the BBB. We report that the cocultivation of astrocytes and cerebrovascular endothelial cells potentiates astrocytic PAI-1 gene expression, and that this response is more pronounced in the presence of pro-inflammatory stimuli, e.g., lipopolysaccharide. These findings imply an important role for intercellular signalling between astrocytes and endothelial cells in the modulation of t-PA activity within the BBB. As it has been shown that genetic variants, i.e. polymorphisms, at the t-PA and the PAI-1 loci affect the expression of these genes in endothelial cells, we investigated whether this is also the case in the brain. Allele-specific gene expression analyses revealed that polymorphisms located in the regulatory regions of the t-PA and the PAI-1 genes affect their expression in human brain tissue and in human astrocytes, respectively. Furthermore, protein-DNA interaction studies demonstrated an altered binding of transcription factors to the polymorphic sites, which likely serves as the molecular genetic explanation behind these…

Subjects/Keywords: gene expression; astrocytes; blood-brain barrier; plasminogen activator inhibitor type-1; polymorphisms; protease nexin-1; tissue-type plasminogen activator; transcriptional regulation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hultman, K. (2010). On the Regulation of the Serine Protease t-PA and its Inhibitor PAI-1 in the Brain. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/22903

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hultman, Karin. “On the Regulation of the Serine Protease t-PA and its Inhibitor PAI-1 in the Brain.” 2010. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed April 16, 2021. http://hdl.handle.net/2077/22903.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hultman, Karin. “On the Regulation of the Serine Protease t-PA and its Inhibitor PAI-1 in the Brain.” 2010. Web. 16 Apr 2021.

Vancouver:

Hultman K. On the Regulation of the Serine Protease t-PA and its Inhibitor PAI-1 in the Brain. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2010. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/2077/22903.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Hultman K. On the Regulation of the Serine Protease t-PA and its Inhibitor PAI-1 in the Brain. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2010. Available from: http://hdl.handle.net/2077/22903

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Rockefeller University

22. Noel-Castro, Melissa. Novel Roles for the Tissue Plasminogen Activator System in the Development of Fetal Alcohol Syndrome and the Regulation of Contextual Learning After Stress.

Degree: 2009, Rockefeller University

URL: https://digitalcommons.rockefeller.edu/student_theses_and_dissertations/121

► Ethanol exposure during synaptogenesis can result in brain and behavior neurotoxic defects referred to as fetal alcohol syndrome (FAS). Since tissue plasminogen activator (tPA) has… (more)

▼ Ethanol exposure during synaptogenesis can result in brain and behavior neurotoxic defects referred to as fetal alcohol syndrome (FAS). Since tissue plasminogen activator (tPA) has been implicated in mediating excitotoxic neurodegeneration we subjected neonatal WT and tPA-/- to an acute ethanol paradigm that serves as a model of FAS. We observed persistent upregulation of tPA and extensive neurodegeneration after ethanol in the forebrain of WT. However, tPA-/- mice were protected from neuronal death, suggesting tPA mediates ethanol-induced neurodegeneration and FAS in mice. Commensurate with neuronal death, we observed ethanol-induced cognitive impairments in adult WT, but not tPA-/- mice. To understand how ethanol affects tPA we subjected mice to drugs that mimic the actions of ethanol in the brain. tPA-/- mice were protected from neurodegeneration after treatment with NMDA-R antagonist, but not after GABAA-agonist, suggesting tPA acts via an NMDA-R mediated mechanism. We also investigated the role of the tPA inhibitor plasminogen activator inhibitor-1 (PAI-1) in FAS. We observed PAI-1-/- mice were more vulnerable to ethanol-induced neurodegeneration than WT mice. In addition, we found that tPA-/-:PAI-1+/- mice treated with ethanol showed increased neurodegeneration than tPA-/- mice. These results suggest PAI-1 is involved in neuronal survival after ethanol. Finally, we explored the role of tPA in hippocampal synaptic plasticity after chronic stress. We restrained WT, tPA-/-, and PAI-1-/- mice for 21 days. We found chronic stress increased tPA activity in WT and PAI-1-/- mice. Stress greatly reduced PAI-1 below baseline levels in WT mice. These stress-induced changes in tPA activity and PAI-1 resulted in decreased contextual fear conditioning in WT and PAI-1-/- mice. Chronic stress did not affect contextual learning in the tPA-/- mice. These results suggest tPA is necessary for the synaptic plasticity cascade that causes cognitive deficits after chronic stress exposure.

Subjects/Keywords: fetal alcohol syndrome; ethanol; plasminogen activator inhibitor-1 (PAI-1); tissue plasminogen activator (tPA); Life Sciences

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Noel-Castro, M. (2009). Novel Roles for the Tissue Plasminogen Activator System in the Development of Fetal Alcohol Syndrome and the Regulation of Contextual Learning After Stress. (Masters Thesis). Rockefeller University. Retrieved from https://digitalcommons.rockefeller.edu/student_theses_and_dissertations/121

Chicago Manual of Style (16^th Edition):

Noel-Castro, Melissa. “Novel Roles for the Tissue Plasminogen Activator System in the Development of Fetal Alcohol Syndrome and the Regulation of Contextual Learning After Stress.” 2009. Masters Thesis, Rockefeller University. Accessed April 16, 2021. https://digitalcommons.rockefeller.edu/student_theses_and_dissertations/121.

MLA Handbook (7^th Edition):

Noel-Castro, Melissa. “Novel Roles for the Tissue Plasminogen Activator System in the Development of Fetal Alcohol Syndrome and the Regulation of Contextual Learning After Stress.” 2009. Web. 16 Apr 2021.

Vancouver:

Noel-Castro M. Novel Roles for the Tissue Plasminogen Activator System in the Development of Fetal Alcohol Syndrome and the Regulation of Contextual Learning After Stress. [Internet] [Masters thesis]. Rockefeller University; 2009. [cited 2021 Apr 16]. Available from: https://digitalcommons.rockefeller.edu/student_theses_and_dissertations/121.

Council of Science Editors:

Noel-Castro M. Novel Roles for the Tissue Plasminogen Activator System in the Development of Fetal Alcohol Syndrome and the Regulation of Contextual Learning After Stress. [Masters Thesis]. Rockefeller University; 2009. Available from: https://digitalcommons.rockefeller.edu/student_theses_and_dissertations/121

University of Michigan

23. Fahim, Abigail T. Directed evolution and in vivo function of plasminogen activator inhibitor-1.

Degree: PhD, Molecular biology, 2007, University of Michigan

URL: http://hdl.handle.net/2027.42/126683

► Plasminogen Activator Inhibitor-1 (PAI-1) is a member of the Serine Protease Inhibitor (SERPIN) family and an important regulator of fibrinolysis. Although similar in structure and… (more)

Subjects/Keywords: Directed Evolution; Function; Pai-1; Plasminogen Activator Inhibitor-1; Serpine1; Thrombosis; Vivo

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Fahim, A. T. (2007). Directed evolution and in vivo function of plasminogen activator inhibitor-1. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/126683

Chicago Manual of Style (16^th Edition):

Fahim, Abigail T. “Directed evolution and in vivo function of plasminogen activator inhibitor-1.” 2007. Doctoral Dissertation, University of Michigan. Accessed April 16, 2021. http://hdl.handle.net/2027.42/126683.

MLA Handbook (7^th Edition):

Fahim, Abigail T. “Directed evolution and in vivo function of plasminogen activator inhibitor-1.” 2007. Web. 16 Apr 2021.

Vancouver:

Fahim AT. Directed evolution and in vivo function of plasminogen activator inhibitor-1. [Internet] [Doctoral dissertation]. University of Michigan; 2007. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/2027.42/126683.

Council of Science Editors:

Fahim AT. Directed evolution and in vivo function of plasminogen activator inhibitor-1. [Doctoral Dissertation]. University of Michigan; 2007. Available from: http://hdl.handle.net/2027.42/126683

24. Salvarani, Mariana [UNESP]. Biomarcadores moleculares relacionados à presença de acidente vascular encefálico e síndrome torácica aguda em anemia falciforme.

Degree: 2017, Universidade Estadual Paulista (UNESP)

URL: http://hdl.handle.net/11449/149929

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

A Anemia Falciforme (AF) é caracterizada pela presença da hemoglobina S em homozigose (Hb SS). As pessoas com AF frequentemente apresentam manifestações clínicas relacionadas a processos de vaso-oclusão como o acidente vascular encefálico (AVE) e síndrome torácica aguda (STA). A regulação da vasoconstrição e vasodilatação é um fator importante na modulação destas manifestações clínicas, sendo alvo de estudos. Neste trabalho, os polimorfismos nos genes de duas enzimas – enzima conversora de angiotensina 1 e 2 (ECA1 e ECA2) e o polimorfismo do inibidor do ativador do plasminogênio tipo 1, relacionado com a fibrinólise, foram avaliados. O Sistema Renina-Angiotensina-Aldosterona atua na manutenção da pressão arterial e do volume sanguíneo por meio do equilíbrio hídrico e eletrolítico e regulação do tônus vascular. A ECA 1 é a principal enzima desse sistema, e cliva a Angiotensina I em Angiotensina II, um potente vasoconstritor. Uma enzima homóloga, a ECA 2, é capaz de clivar a Angiotensina II em Angiotensina 1-7, uma vasodilatadora. Os polimorfismos I/D no gene ECA1 (rs1799752) e A/G (rs2106809) no gene ECA2 foram estudados neste trabalho. Além disso, a regulação fibrinolítica também está relacionada às manifestações clínicas na AF. O inibidor do ativador do plasminogênio tipo 1 (PAI-1) é um regulador da fibrinólise, inibindo os ativadores do plasminogênio e a formação de plasmina, responsável pela degradação do coágulo. O polimorfismo mais estudado no gene PAI1, de inserção de uma guanina (4G/5G) (rs1799889) na região promotora do gene, aumenta a atividade de enzima e diminui a ação fibrinolítica. Para verificar se estes polimorfismos estão relacionados à presença das manifestações clínicas, STA e AVE, foram genotipadas 392 pessoas com AF. As amostras foram caracterizadas segundo seu perfil hemoglobínico, e submetidas à extração de DNA, e utilizadas para a detecção dos polimorfismos por PCR-RFLP. As frequências dos polimorfismos foram analisadas em conjunto com as informações de ocorrência das manifestações clínicas, que foram obtidas dos prontuários médicos. O genótipo mais frequente encontrado para o polimorfismo I/D no gene ECA1 foi o heterozigoto ID (47,2%) e o alelo mais frequente foi o D (57,3%). Para o polimorfismo A/G no gene ECA2 o genótipo mais frequente foi o homozigoto GG (45,3%) entre as mulheres, e o alelo…

Advisors/Committee Members: Universidade Estadual Paulista (UNESP), Domingos, Claudia Regina Bonini [UNESP].

Subjects/Keywords: Vaso-oclusão; Polimorfismo; Enzima conversora de angiotensina; Inibidor do ativador do plasminogênio tipo 1; Vaso-occlusion; Plasminogen activator inhibitor type 1; Polymorphism; Angiotensin-converting enzyme

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Salvarani, M. [. (2017). Biomarcadores moleculares relacionados à presença de acidente vascular encefálico e síndrome torácica aguda em anemia falciforme. (Masters Thesis). Universidade Estadual Paulista (UNESP). Retrieved from http://hdl.handle.net/11449/149929

Chicago Manual of Style (16^th Edition):

Salvarani, Mariana [UNESP]. “Biomarcadores moleculares relacionados à presença de acidente vascular encefálico e síndrome torácica aguda em anemia falciforme.” 2017. Masters Thesis, Universidade Estadual Paulista (UNESP). Accessed April 16, 2021. http://hdl.handle.net/11449/149929.

MLA Handbook (7^th Edition):

Salvarani, Mariana [UNESP]. “Biomarcadores moleculares relacionados à presença de acidente vascular encefálico e síndrome torácica aguda em anemia falciforme.” 2017. Web. 16 Apr 2021.

Vancouver:

Salvarani M[. Biomarcadores moleculares relacionados à presença de acidente vascular encefálico e síndrome torácica aguda em anemia falciforme. [Internet] [Masters thesis]. Universidade Estadual Paulista (UNESP); 2017. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/11449/149929.

Council of Science Editors:

Salvarani M[. Biomarcadores moleculares relacionados à presença de acidente vascular encefálico e síndrome torácica aguda em anemia falciforme. [Masters Thesis]. Universidade Estadual Paulista (UNESP); 2017. Available from: http://hdl.handle.net/11449/149929

25. Qureshi, Tihami. From Loop to Strand: Characterization of the Conformation and Dynamics of the Human Plasminogen Activator Inhibitor-1 Reactive Center.

Degree: 2013, University of Tennessee – Knoxville

URL: https://trace.tennessee.edu/utk_graddiss/2470

► Plasminogen activator inhibitor-1 (PAI-1), with its cofactor vitronectin (VN), controls the rate of plasmin-mediated fibrin breakdown in blood clots by inhibiting tissue-plasminogen activator (tPA) and… (more)

▼ Plasminogen activator inhibitor-1 (PAI-1), with its cofactor vitronectin (VN), controls the rate of plasmin-mediated fibrin breakdown in blood clots by inhibiting tissue-plasminogen activator (tPA) and urokinase-plasminogen activator (uPA). The activity of PAI-1 is attributed to its reactive center loop (RCL), which is solvent-exposed in an active conformation, but inserts as an additional strand into its central β [beta]-sheet during transition to a latent state and during inhibition. VN slows the latency transition, and the rate at which PAI-1 inhibits the plasminogen activators (PAs) also differs. However, the steps during the latency transition, mechanism of VN stabilization, and basis for inhibitory rate differences are unclear, and all involve the RCL. To address these issues, this study combines computational methods with cysteine-scanning mutagenesis of the RCL for fluorescence and electron paramagnetic resonance (EPR) spectroscopy to investigate changes in the RCL due to interactions with these ligands. Homology modeling of the RCL indicates sampling of a limited energy-conformation landscape for this region. Fluorescence investigation of the latency transition suggest that RCL detachment to assume the latent conformation occurs within the first 10 minutes of the process, which typically has a half-life of about 1 hour. Equilibrium-binding studies indicate that VN, its N-terminal somatomedin B (SMB) domain, and a longer truncation involving an intrinsically disordered domain (SMB-IDD) increase the solvent exposure of the RCL in stabilizing PAI-1. Studies with active site-blocked PAs reveal that both dock at the RCL, but rest differently on its top, employing distinct exosite interactions and mobility constraints on the RCL that likely effect the kinetics of its interaction with PAI-1. Thereby, this study provides detailed structural information on the PAI-1 RCL, and new insights into the latency process and interaction with PAs. Such information is valuable in the development of inhibitors specific for the interaction of PAI-1 with either PA, and in targeting this biomarker in diseases states caused by the dysregulation of PAI-1. Overall, the results from this work reveal that ligand interactions fine-tune the activity of PAI-1 by affecting the conformation and dynamics of the RCL from its position as a solvent-exposed loop to an inserted β [beta]-strand.

Subjects/Keywords: Plasminogen activator inhibitor-1; vitronectin; tissue-plasminogen activator; urokinase-plasminogen activator; fluorescence; electron paramagnetic resonance; Biochemistry, Biophysics, and Structural Biology

…Plasminogen activator inhibitor-1 PEG Polyethylene glycol Plg Plasminogen Pln Plasmin QY… …activator inhibitor-1 (PAI-1), discovered in the 1970s and found only in vertebrates… …Conformational State & Presence of Cofactor on PAI-1 Inhibition of Plasminogen Activators 14 Table… …Plasminogen Activators 2 Figure 1.2 Multiple Signaling Pathways Are Involved in PAI-1 Expression… …Stabilization of PAI-1 102 Figure 3.4 VN & Heparin Make PAI-1 A More Efficient Thrombin Inhibitor…

10 more images…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Qureshi, T. (2013). From Loop to Strand: Characterization of the Conformation and Dynamics of the Human Plasminogen Activator Inhibitor-1 Reactive Center. (Doctoral Dissertation). University of Tennessee – Knoxville. Retrieved from https://trace.tennessee.edu/utk_graddiss/2470

Chicago Manual of Style (16^th Edition):

Qureshi, Tihami. “From Loop to Strand: Characterization of the Conformation and Dynamics of the Human Plasminogen Activator Inhibitor-1 Reactive Center.” 2013. Doctoral Dissertation, University of Tennessee – Knoxville. Accessed April 16, 2021. https://trace.tennessee.edu/utk_graddiss/2470.

MLA Handbook (7^th Edition):

Qureshi, Tihami. “From Loop to Strand: Characterization of the Conformation and Dynamics of the Human Plasminogen Activator Inhibitor-1 Reactive Center.” 2013. Web. 16 Apr 2021.

Vancouver:

Qureshi T. From Loop to Strand: Characterization of the Conformation and Dynamics of the Human Plasminogen Activator Inhibitor-1 Reactive Center. [Internet] [Doctoral dissertation]. University of Tennessee – Knoxville; 2013. [cited 2021 Apr 16]. Available from: https://trace.tennessee.edu/utk_graddiss/2470.

Council of Science Editors:

Qureshi T. From Loop to Strand: Characterization of the Conformation and Dynamics of the Human Plasminogen Activator Inhibitor-1 Reactive Center. [Doctoral Dissertation]. University of Tennessee – Knoxville; 2013. Available from: https://trace.tennessee.edu/utk_graddiss/2470

North-West University

26. North, Christina Johanna. Effect of dietary fibre on selected haemostatic variables and C-reactive protein / Christina Johanna North .

Degree: 2006, North-West University

URL: http://hdl.handle.net/10394/1417

► Motivation: Cardiovascular heart disease (CVD) is the leading cause of death worldwide. Risk markers for CVD include, amongst others, the haemostatic factors tissue-type plasminogen activator… (more)

▼ Motivation: Cardiovascular heart disease (CVD) is the leading cause of death worldwide. Risk markers for CVD include, amongst others, the haemostatic factors tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor type 1 (PAI-1), factor VII (FVII) and fibrinogen and more recently, C-reactive protein (CRP), a sensitive marker of inflammation. Epidemiological studies have demonstrated an inverse association between dietary fibre (DF) consumption and risk factors for CVD and CVD prevalence. Some research indicates that this protection may be related to favourable changes in the haemostatic profile and inflammatory markers. This is applicable for the consumption of total DF, as well as soluble and insoluble fibre. However, clinical intervention trials report conflicting data on the effects of DF on t-PA, PAI-1, FVII, fibrinogen and CRP. In addition, available literature is not clear on the mechanisms through which DF may have favourable effects. Objective: The main objective of this study was to review the results of randomised controlled trials systematically on the effects of DF on the above-mentioned selected haemostatic variables and CRP in healthy adults and subjects with hypertriglyceridaemia and the metabolic syndrome. Methods: Human adult intervention trials, at least two weeks in duration, with an increased and measurable consumption of DF were included. Electronic databases were searched from the earliest record to May/July 2006 and supplemented by crosschecking reference lists of relevant publications. From the literature search, two reviewers identified studies that were rated for quality based on the published methodology. No formal statistical analysis was performed due to the large differences in the study designs of the dietary intervention trials. The primary outcome measures were percentage changes between intervention and control groups, or baseline to end comparisons for t-PA, PAI-1, FVII, fibrinogen and CRP. Results t-PA activity increased significantly (14-167%) over the short and long-term following increased fibre intakes. PAI-1 activity decreased significantly between 15-57% over periods ranging from two to six weeks. These favourable changes in t-PA and PAI-1 occurred in healthy, hypertriglyceridaemic and metabolic syndrome subjects following consumption of diets containing ≥3.3 g/MJ DF and ≥4.5 g/MJ DF respectively. Mechanisms through which DF may affect t-PA and PAI-1 include its lowering effect on insulinaemic and glycaemic responses, decreasing triglycerides which are a precursor of very-low-density lipoproteins, fermentation of DF to short-chain fatty acids, which may reduce free fatty acid concentrations, as well as the role of DF in promoting weight loss. High DF intakes did not have a significant effect on fibrinogen concentrations possibly because of relatively little weight loss, too low DF dosages and maintaining a good nutritional status. Inadequate study designs deterred from meaningful conclusions. Significant decreases in FVll coagulant activity (6-16%)…

Subjects/Keywords: Dietary fibre; Tissue-type plasminogen activator; Plasminogen activator inhibitor type 1; Factor VII; Fibrinogen; C-reactive protein; Systematic review

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

North, C. J. (2006). Effect of dietary fibre on selected haemostatic variables and C-reactive protein / Christina Johanna North . (Thesis). North-West University. Retrieved from http://hdl.handle.net/10394/1417

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

North, Christina Johanna. “Effect of dietary fibre on selected haemostatic variables and C-reactive protein / Christina Johanna North .” 2006. Thesis, North-West University. Accessed April 16, 2021. http://hdl.handle.net/10394/1417.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

North, Christina Johanna. “Effect of dietary fibre on selected haemostatic variables and C-reactive protein / Christina Johanna North .” 2006. Web. 16 Apr 2021.

Vancouver:

North CJ. Effect of dietary fibre on selected haemostatic variables and C-reactive protein / Christina Johanna North . [Internet] [Thesis]. North-West University; 2006. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/10394/1417.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

North CJ. Effect of dietary fibre on selected haemostatic variables and C-reactive protein / Christina Johanna North . [Thesis]. North-West University; 2006. Available from: http://hdl.handle.net/10394/1417

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Gothenburg / Göteborgs Universitet

27. Ridderstråle, Wilhelm. Blood Pressure Elevation - Impact on Cardiovascular Structure and Endogenous Fibrinolysis.

Degree: 2008, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/10130

► Blood pressure elevation is a major risk factor for cardiovascular events and the risk increases in a dose-dependant manner. It is of importance to identify… (more)

▼ Blood pressure elevation is a major risk factor for cardiovascular events and the risk increases in a dose-dependant manner. It is of importance to identify subjects prone to develop hypertension and adverse cardiovascular remodeling in order to start treatment timely. The increased risk of myocardial infarction and ischemic stroke in hypertension suggests that the condition is associated with prothrombotic mechanisms. Our research group recently discovered that the capacity for activation of the endogenous fibrinolytic system by acute release of tissue plasminogen activator (t-PA) is markedly impaired in subjects with hypertension. This impairment could contribute to the increased risk for atherothrombotic events. The predictive value of blood pressure elevation (SBP 140-160 and/or DBP 85-95 mmHg; BPE group) or normal blood pressure (SBP 110-130 and DBP 60-80 mmHg; NC group) was studied in a cohort of 20-year old men investigated in 1987. The prevalence of hypertension was 74.5% and 5.9% in the BPE and NC group, respectively, at 20 year follow-up. The difference in blood pressure level at baseline between the groups contrasted even more at follow-up. Further, the BPE group had significantly increased left ventricular mass index and intima-media thickness compared to the NC group. We investigated if the impaired fibrinolytic capacity in untreated hypertension could be restored by chronic and acute blood pressure lowering. T-PA release was stimulated by infusion of substance P in the perfused-forearm model before and during chronic and acute blood pressure lowering. Chronic antihypertensive treatment with either the calcium antagonist felodipine or the ACE-inhibitor lisinopril, increased the amount of t-PA released and improved the rapidity of the t-PA response. Changes were similar in the two treatment groups, suggesting the improvement to be related to the blood pressure lowering per se. However, acute blood pressure lowering with intravenous sodium nitroprusside did not affect the stimulated t-PA release. The results of the two studies indicate that high blood pressure decreases the cellular content of t-PA, rather than interfering with the release mechanisms of the protein. Further, we explored the impact of the tensile force component of blood pressure on the regulation of fibrinolytic proteins by studying cultured endothelial cells in an in vitro biomechanical experimental model. Prolonged cyclic strain, mimicking the hypertensive state, was found to suppress t-PA gene expression and protein secretion. In contrast, the main inhibitor of t-PA, plasminogen activator inhibitor-1 was induced, adding to the negative effects of elevated blood pressure on fibrinolysis. In conclusion, blood pressure elevation in young age predicts adverse cardiovascular remodeling and hypertension twenty years later. Hypertension increases the risk of atherothrombotic events by impaired fibrinolysis, possibly through a direct inhibitory effect on t-PA expression by enhanced tensile stress. Chronic blood pressure lowering restores the…

Subjects/Keywords: hypertension; left ventricular hypertrophy; intima-media thickness; fibrinolysis; endothelium; tissue plasminogen activator; antihypertensive agents; mechanical stress; plasminogen activator inhibitor-1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ridderstråle, W. (2008). Blood Pressure Elevation - Impact on Cardiovascular Structure and Endogenous Fibrinolysis. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/10130

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Ridderstråle, Wilhelm. “Blood Pressure Elevation - Impact on Cardiovascular Structure and Endogenous Fibrinolysis.” 2008. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed April 16, 2021. http://hdl.handle.net/2077/10130.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Ridderstråle, Wilhelm. “Blood Pressure Elevation - Impact on Cardiovascular Structure and Endogenous Fibrinolysis.” 2008. Web. 16 Apr 2021.

Vancouver:

Ridderstråle W. Blood Pressure Elevation - Impact on Cardiovascular Structure and Endogenous Fibrinolysis. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2008. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/2077/10130.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Ridderstråle W. Blood Pressure Elevation - Impact on Cardiovascular Structure and Endogenous Fibrinolysis. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2008. Available from: http://hdl.handle.net/2077/10130

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Gothenburg / Göteborgs Universitet

28. Hrafnkelsdóttir, Thórdís Jóna 1965-. Local regulation of the endogenous fibrinolytic system in man.

Degree: 2001, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/15302

► The physiologically most important activator of intravascular fibrinolysis is tissue-type plasminogen activator (tPA). The endothelium synthesises and stores tPA and regulated release of the enzyme… (more)

▼ The physiologically most important activator of intravascular fibrinolysis is tissue-type plasminogen activator (tPA). The endothelium synthesises and stores tPA and regulated release of the enzyme is an important mechanism for removal of fibrin from blood vessels. Plasminogen activator inhibitor type-1 (PAI-1) is the main inhibitor of tPA. The aim of the present thesis was to study how the local availability of free tPA is regulated under baseline conditions and during stimulated tPA release, to explore the potential role of extracellular nucleotides as potential mediators of tPA release in tissue injury and ischaemia, and to analyse if the capacity for tPA is decreased in hypertension and advanced chronic renal failure, and if so which mechanism may be involved.The studies were performed in 115 healthy subjects, seven patients with essential hypertension, and nine patients with advanced chronic renal failure. The release of tPA and PAI-1 was studied in a perfused-forearm model, at baseline and during stimulation with sodium nitroprusside, methacholine, desmopressin, or the extracellular nucleotides ATP and UTP. Also, the synthesis and secretion of tPA were studied in human conduit vessels perfused with high versus low intraluminal pressure ex vivo. During the morning hours the fibrinolytic activity increased secondary to an increase in the endothelial release of tPA and a decrease in the overall availability of its inhibitor PAI-1. The capacity for stimulated tPA release was not predicted from either plasma concentrations of the activator or its inhibitor, or from the basal release rate of these proteins. The local availability of free active tPA during stimulation of tPA release was dependent on the tPA release rate and not the inflow/release of inhibitors (PAI-1). The extracellular nucleotides ATP and UTP were found to induce regulated tPA release, which in the case of UTP was independent of NO and prostaglandin synthesis. Nucleotide stimulated tPA release may be a potential mechanism for activation of the thromboprotective programme.The capacity for regulated tPA release was found to be markedly impaired in patients with hypertension and advanced chronic renal failure. A potential mechanism is that high blood pressure in it self impairs regulated tPA release, as high intraluminal perfusions pressure inhibited tPA synthesis and release in endothelial cells ex vivo.In conclusion, these findings support the hypothesis that regulated tPA release is the major determinant of the local availability of active tPA. It was therefore of interest to find the capacity for stimulated tPA release to be reduced in patients with hypertension and advanced chronic renal failure, an impairment that potentially increases the susceptibility for atherothrombosis.

Subjects/Keywords: tissue-type plasminogen activator; plasminogen activator inhibitor type-1; endothelium; extracellular nucleotides; hypertension; chronic renal failure

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hrafnkelsdóttir, T. J. 1. (2001). Local regulation of the endogenous fibrinolytic system in man. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/15302

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hrafnkelsdóttir, Thórdís Jóna 1965-. “Local regulation of the endogenous fibrinolytic system in man.” 2001. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed April 16, 2021. http://hdl.handle.net/2077/15302.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hrafnkelsdóttir, Thórdís Jóna 1965-. “Local regulation of the endogenous fibrinolytic system in man.” 2001. Web. 16 Apr 2021.

Vancouver:

Hrafnkelsdóttir TJ1. Local regulation of the endogenous fibrinolytic system in man. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2001. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/2077/15302.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Hrafnkelsdóttir TJ1. Local regulation of the endogenous fibrinolytic system in man. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2001. Available from: http://hdl.handle.net/2077/15302

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Gothenburg / Göteborgs Universitet

29. Tjärnlund Wolf, Anna 1974-. On the Tissue-type Plasminogen Activator (t-PA) -7,351C>T Enhancer Polymorphism. Importance for endothelial t-PA gene expression and arterial thrombotic disease.

Degree: 2004, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/16258

► Local endothelial release of tissue-type plasminogen activator (t-PA) is an important thromboprotective mechanism. Earlier work by our group has identified a common single nucleotide polymorphism… (more)

▼ Local endothelial release of tissue-type plasminogen activator (t-PA) is an important thromboprotective mechanism. Earlier work by our group has identified a common single nucleotide polymorphism (SNP) at the t-PA locus (-7,351C>T), located within a GC-box in the retinoic acid (RA) and steroid hormone responsive t-PA enhancer. This SNP was associated with local t-PA release in vivo, as subjects homozygous for the wild-type -7,351C allele had twice the t-PA release rates compared to carriers of the mutant T allele. The aim of the present thesis was to elucidate the physiological and pathophysiological relevance of this t-PA variant. TaqMan genotyping assays were designed for a set of SNPs in hemostatic genes to facilitate association studies on these SNPs and thrombotic disease. Specificity and reproducibility was confirmed by DNA sequencing and repeated genotyping. The pathophysiologial relevance of the t-PA -7,351C>T SNP was initially addressed in a prospective study on myocardial infarction (MI) in northern Sweden. An independent association for the t-PA -7,351C>T SNP was found, with a greater risk of MI in T allele carriers. In a large case-control study on ischemic stroke from western Sweden we did, however, not detect a similar association. This study also included a genetic variant of the main inhibitor of t-PA, the plasminogen activator inhibitor type-1 (PAI-1) -675 4G>5G SNP. A reduced risk of ischemic stroke was observed for the combined t-PA CC and PAI-1 4G4G genotype.In vitro studies were performed to functionally characterize the t-PA -7,351C>T SNP. Gel shift analysis using nuclear extracts derived form various cell types, including endothelial cells (ECs) and neuronal-like cells, revealed a strongly reduced binding affinity of transcription factors Sp1 and Sp3 to the T allele, which is interesting in view of the role for Sp1 in gene regulation and enhancer action. Transient transfections demonstrated a lower transcriptional activity in the T enhancer variant after stimulation with RA. An interaction between Sp1 and the RA receptor was also observed. ECs carrying the T allele showed a reduced t-PA induction, both at the mRNA and protein level, in response to RA and protein kinase C (PKC) activation. The combination of RA and PKC activation produced a synergistic t-PA response, resulting in a 2-fold difference in t-PA expression between genotypes.In conclusion, the t-PA -7,351C>T SNP affects endothelial t-PA gene expression at the level of transcription. The reduced expression seen with the mutant T allele may explain our finding of an increased risk for MI in individuals carrying this allele. The t-PA -7,351C>T SNP did not show a significant association to ischemic stroke, but a reduced risk was observed in subjects with the combined t-PA CC and PAI-1 4G4G genotype, supporting a differentiated and more complex role for t-PA and PAI-1 in the brain as compared to the heart.

Subjects/Keywords: tissue-type plasminogen activator; plasminogen activator inhibitor type-1; polymorphism; endothelium; Sp1; gene expression; myocardial infarction; ischemic stroke

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Tjärnlund Wolf, A. 1. (2004). On the Tissue-type Plasminogen Activator (t-PA) -7,351C>T Enhancer Polymorphism. Importance for endothelial t-PA gene expression and arterial thrombotic disease. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/16258

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Tjärnlund Wolf, Anna 1974-. “On the Tissue-type Plasminogen Activator (t-PA) -7,351C>T Enhancer Polymorphism. Importance for endothelial t-PA gene expression and arterial thrombotic disease.” 2004. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed April 16, 2021. http://hdl.handle.net/2077/16258.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Tjärnlund Wolf, Anna 1974-. “On the Tissue-type Plasminogen Activator (t-PA) -7,351C>T Enhancer Polymorphism. Importance for endothelial t-PA gene expression and arterial thrombotic disease.” 2004. Web. 16 Apr 2021.

Vancouver:

Tjärnlund Wolf A1. On the Tissue-type Plasminogen Activator (t-PA) -7,351C>T Enhancer Polymorphism. Importance for endothelial t-PA gene expression and arterial thrombotic disease. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2004. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/2077/16258.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Tjärnlund Wolf A1. On the Tissue-type Plasminogen Activator (t-PA) -7,351C>T Enhancer Polymorphism. Importance for endothelial t-PA gene expression and arterial thrombotic disease. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2004. Available from: http://hdl.handle.net/2077/16258

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

North-West University

30. Palmer, Iolanthe Marike. The association of uric acid and plasminogen activator inhibitor-1 (PAI-1) with cardiovascular function in South African women : the POWIRS-study / I.M. Palmer .

Degree: 2006, North-West University

URL: http://hdl.handle.net/10394/117

► Motivation: Hypertension is a fast growing health risk, leading to increased incidences of cardiovascular dysfunction and mortality. However, the prevalence of hypertension is higher in… (more)

▼ Motivation: Hypertension is a fast growing health risk, leading to increased incidences of cardiovascular dysfunction and mortality. However, the prevalence of hypertension is higher in some ethnic populations than others. Several South African studies have found that the African population is more susceptible to the development of hypertension, compared to the Caucasian population. Cardiovascular dysfunction is often accompanied by elevated levels of uric acid (UA) and plasminogen activator inhibitor-I (PAI-1) and both are factors associated with the metabolic syndrome. A lack of data regarding the association of UA and PAL1 with cardiovascular dysfunction in a South African context, serves as a motivation for conducting this study. Objective: To determine the association of UA and PAI-1 with cardiovascular dysfunction in African and Caucasian women from South Africa. Methodology: The manuscript presented in Chapter 2 made use of the data obtained in the POWIRS (Profiles of Obese Women with the Insulin Resistance Syndrome) study. A group of 102 African women and 115 Caucasian women, living in the North West Province of South Africa, were recruited according to their body mass indexes. The groups were divided into lean, overweight and obese according to their body mass index. Anthropometric and cardiovascular measurements were taken and determinations were done of their blood lipid profiles, UA. PAI-1, fasting insulin and glucose levels, HOMA-IR (homeostasis model assessment-insulin resistance) and leptin levels. The subject's total dietary protein intake was determined by means of a dietary questionnaire. Comparisons between the groups were done using an independent t-test as well as a multiple analysis of covariance (MANCOVA) whilst adjusting for certain variables. Each ethnic group was divided into UA and PAI-1 tertiles, for comparison between the 1" and 3' tertiles. Correlation ~0efIi~ientS were determined to show any associations between UA and PAI-1 with cardiovascular variables as well as variables associated with the metabolic syndrome. Forward stepwise multiple regression analyses were performed using UA and PAL1 respectively as dependent variables. The study was approved by the Ethics committee of the North-West University and all the subjects gave informed consent in writing. The reader is referred to the experimental procedure section in Chapter 2 for a more detailed description of the subjects, study design and analytical procedures used in this dissertation. Results and conclusion: Results from the POWIRS-study showed that despite the African women's higher blood pressure, they had significantly lower levels of UA and PAI-I compared to the Caucasian women. Although the Caucasian women had significantly higher circulating levels of UA and PAI-1, they showed no sign of cardiovascular dysfunction. The detrimental effects might, however, become more noticeable with an increase in age. From this study it is concluded that UA and PAL1 is not associated with the increased…

Subjects/Keywords: Uric acid; Plasminogen activator inhibitor-1; Cardiovascualr dysfunction; African women; Caucasian women

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APA (6^th Edition):

Palmer, I. M. (2006). The association of uric acid and plasminogen activator inhibitor-1 (PAI-1) with cardiovascular function in South African women : the POWIRS-study / I.M. Palmer . (Thesis). North-West University. Retrieved from http://hdl.handle.net/10394/117

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Palmer, Iolanthe Marike. “The association of uric acid and plasminogen activator inhibitor-1 (PAI-1) with cardiovascular function in South African women : the POWIRS-study / I.M. Palmer .” 2006. Thesis, North-West University. Accessed April 16, 2021. http://hdl.handle.net/10394/117.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Palmer, Iolanthe Marike. “The association of uric acid and plasminogen activator inhibitor-1 (PAI-1) with cardiovascular function in South African women : the POWIRS-study / I.M. Palmer .” 2006. Web. 16 Apr 2021.

Vancouver:

Palmer IM. The association of uric acid and plasminogen activator inhibitor-1 (PAI-1) with cardiovascular function in South African women : the POWIRS-study / I.M. Palmer . [Internet] [Thesis]. North-West University; 2006. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/10394/117.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Palmer IM. The association of uric acid and plasminogen activator inhibitor-1 (PAI-1) with cardiovascular function in South African women : the POWIRS-study / I.M. Palmer . [Thesis]. North-West University; 2006. Available from: http://hdl.handle.net/10394/117

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

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