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Dissertations / Theses on the topic 'Dysfunctional protest'

Author: Grafiati

Published: 7 June 2025

Last updated: 2 August 2025

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1

Faggian, Alessia. "Glucotoxicity, Protein Glycation and Adipose Tissue Dysfunction." Doctoral thesis, Università degli studi di Padova, 2016. http://hdl.handle.net/11577/3425305.

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Introduction: Glycation is a non-enzymatic reaction between a sugar and a free-amino group contained in molecules such as proteins, amino acids, DNA, RNA, and lipids. In the initial phase, the carbonyl group of the reducing carbohydrate condenses with the free-amino group on the biomolecule to form a reversible glycosylamine, which is then converted to a more stable Amadori product. Once formed, these products can with time undergo to dehydration, cyclization, oxidation, and rearrangements forming a polymorphic group of compounds collectively referred as Advanced Glycation End-products (AGEs).

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2

Dutt, Tina. "The effect of activated protein C on cardiac cells." Thesis, University of Liverpool, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.631571.

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Activated Protein C (APC) is an endogenous anticoagulant that regulates thrombin generation. Its physiological importance is reflected by the thrombotic phenotype of PC deficient individuals and those with APC resistance due to mutation at the Factor V cleavage site. At a molecular level, thrombin binding to the receptor thrombomodulin (TM) converts endothelial protein C receptor (EPCR) bound PC into APC. APC has a negative feedback role in curbing thrombin generation by inactivating coagulation factors V and VIII. Clinically, acquired PC deficiency occurs in conditions such as severe sepsis a

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3

Adams, Gregory Nicholas. "Prolylcarboxypeptidase protects from vascular dysfunction and promotes vascular repair." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1346973249.

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4

Gianni, Davide. "The role of unfolded protein deposits in cardiac dysfunction." Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/7029.

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In this study we investigated the role of unfolded proteins as a toxic insult for cardiomyocytes in idiopathic dilated cardiomyopathy (DCM). We first confirmed the presence of amyloid fibers in DCM cardiomyocytes by histological and ultrastructural analysis, showing their preferentially intracellular distribution. These molecular species seem to coexist with low-complexity β-folded precursors (oligomers) which in our experiments could promote increase of systolic Ca2+ in normal cardiomyocytes and alterations of contractility. Our results suggest that these molecular species trigger the overexp

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5

Marrerios, Rita [Verfasser]. "Protein homeostasis dysfunction in chronic brain disorders / Rita Marrerios." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2020. http://d-nb.info/1219299618/34.

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6

Del, Dotto Valentina <1987&gt. "OPA1 isoforms and protein domains in the rescue of mitochondrial dysfunctions." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2015. http://amsdottorato.unibo.it/7033/1/Del_Dotto_Valentina_tesi.pdf.

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Mutations in OPA1 gene have been identified in the majority of patients with Dominant Optic Atrophy (DOA), a blinding disease, and the syndromic form DOA-plus. OPA1 protein is a mitochondrial GTPase involved in various mitochondrial functions, present in humans in eight isoforms, resulting from alternative splicing and proteolytic processing. In this study we have investigated the specific role of each isoform through expression in OPA-/- MEFs, by evaluating their ability to improve the defective mitochondrial phenotypes. All isoforms were able to rescue the energetic efficiency, mitochondrial

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Del, Dotto Valentina <1987&gt. "OPA1 isoforms and protein domains in the rescue of mitochondrial dysfunctions." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2015. http://amsdottorato.unibo.it/7033/.

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Mutations in OPA1 gene have been identified in the majority of patients with Dominant Optic Atrophy (DOA), a blinding disease, and the syndromic form DOA-plus. OPA1 protein is a mitochondrial GTPase involved in various mitochondrial functions, present in humans in eight isoforms, resulting from alternative splicing and proteolytic processing. In this study we have investigated the specific role of each isoform through expression in OPA-/- MEFs, by evaluating their ability to improve the defective mitochondrial phenotypes. All isoforms were able to rescue the energetic efficiency, mitochondrial

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8

Chang, Alex Hongsheng. "Intracellular inhibition of immune dysfunction induced by HIV-1 Nef protein." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0017/NQ56524.pdf.

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9

Low, Darryl Weijun. "Synaptic vesicle protein 2A-dependent function and dysfunction at the presynapse." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31320.

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Neurotransmission is essential for neuronal communication. At the presynapse, synaptic vesicles (SVs) undergo exocytosis to release neurotransmitter in response to incoming action potentials, and endocytosis to maintain the supply of SVs needed for further rounds of exocytosis. A key event during SV endocytosis is the efficient sorting and localisation of SV proteins at the plasma membrane. This ensures that nascent SVs that are formed have the correct molecular composition to participate in subsequent exocytic events. The sorting of SV proteins at the plasma membrane is usually facilitated by

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10

Betters, Jenna Leigh Jones. "Trolox supplementation during mechanical ventilation attenuates contractile dysfunction and protein degradation." [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0004290.

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11

Joshi, Mandar S. "Mechanisms of nitric oxide control in endothelial and cardiac dysfunction." Connect to resource, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1124124428.

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12

Pickworth, Josephine. "Links between dysfunctional Bone Morphogenetic Protein signalling and Interleukin-1ß mediated inflammation in pulmonary arterial hypertension." Thesis, University of Sheffield, 2017. http://etheses.whiterose.ac.uk/18607/.

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Rationale: Bone morphogenetic protein receptor type 2 (BMPR2) mutations are present in up to 70% of patients with heritable and up to 25% with idiopathic pulmonary arterial hypertension, however penetrance within families with the same mutation is low implying the necessity for a ‘second hit’. Inflammatory cytokines are raised in patients with PAH, and in animal models have been shown to play a modulating role in disease pathogenesis. Objective: To determine whether there is a pulmonary specific interplay between BMPR2 deficiency and inflammatory Interleukin 1ß (IL-1ß) signalling that may expl

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13

Xu, Yuekang. "Biochemical basis of B cell dysfunction in lyn kinase deficient mice /." Connect to thesis, 2003. http://eprints.unimelb.edu.au/archive/00002881.

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Thesis (Ph.D.)--University of Melbourne, The Walter & Eliza Hall Institute of Medical research, Dept. of Medical Biology, 2004.<br>Typescript (photocopy). Includes bibliographical references (leaves 161-190).

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14

Li, Huiying. "Adipocyte fatty acid-binding protein : a link between inflammation and vascular dysfunction /." Click to view the E-thesis via HKUTO, 2010. http://sunzi.lib.hku.hk/hkuto/record/B44248714.

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15

Labbé, Katherine. "The role of monocyte chemoattractant protein-1 in diaphragm dysfunction during sepsis /." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=101595.

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Sepsis-induced diaphragmatic force loss and failure are associated with an increased exposure to proinflammatory mediators. The septic diaphragm has recently been reported to overexpresse chemokines, including the CC chemokine MCP-1 (monocyte chemoattractant protein-1). This thesis seeks to address the significance of MCP-1 overproduction in diaphragm proinflammatory mediator expression and skeletal muscle contractile function. Neutralization of endogenous MCP-1, produced following administration of LPS, decreased transcription of iNOS, IL-6, IL-1alpha, IL-1beta and MCP-1 in the diaphragm and

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Li, Huiying, and 李慧颖. "Adipocyte fatty acid-binding protein: a link between inflammation and vascular dysfunction." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B44248714.

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17

Peters, Theodore Walter. "Investigating the relationship between protein aggregates and cellular dysfunction in polyglutamine disease /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2008.

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Thesis (Ph.D. in Biochemistry) -- University of Colorado Denver, 2008.<br>Typescript. Includes bibliographical references (leaves 128-144). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;

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18

Etwebi, Zienab. "MYELOPEROXIDASE INDUCES ENDOTHELIAL DYSFUNCTION VIA ACTIVATION OF THE CALCIUM DEPENDENT PROTEASE CALPAIN." Diss., Temple University Libraries, 2018. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/508536.

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Biomedical Sciences<br>Ph.D.<br>Cardiovascular disease and the associated endothelial dysfunction are characterized by leukocyte activation, decrease endothelial nitric oxide synthase (eNOS) activity, and increased endothelial cell adhesion molecules expression. This leads to the release of myeloperoxidase (MPO) by activated neutrophils and monocytes. MPO is a peroxidase enzyme that plays an important role in innate immune host defense, however it has been shown to play a pathogenic role in cardiovascular disease, mainly by causing endothelial dysfunction. The molecular mechanisms through whic

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19

Menazza, Sara. "Relationship between mitochondrial ROS formation and myofibrillar protein oxidation in contractile dysfunction." Doctoral thesis, Università degli studi di Padova, 2011. http://hdl.handle.net/11577/3421607.

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Oxidative stress has been related in numerous cardiovascular and muscular pathologies, but the causal relationship between ROS accumulation and contractile impairment is not clear yet. We hypothesized that upon oxidative stress myofibrillar proteins (MPs) are oxidized providing a relevant contribution to the decrease of contractile performance. The evidence provided in the present work demonstrates the key role of mitochondrial dysfunction in muscle injury. We demonstrated that ROS produced in mitochondria alter MPs causing contractile dysfunction in cardiac and skeletal muscle. These results

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20

Slatculescu, Andreea M. "Immune Dysfunction Associated with Hemodialysis Modalities." Thèse, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/30493.

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Infection is a leading cause of death in hemodialysis patients, partly due to dysfunctional immunity. Frequent dialysis therapy improves patient outcomes and quality of life. We hypothesize that extended home hemodialysis (EHHD) also improves immune function compared to conventional in-hospital hemodialysis (CHD); therefore, we designed a prospective matching-cohort clinical study to assess serum inflammatory markers and the functional capacity of monocyte-derived dendritic cells (MDDCs) and T-lymphocytes. Serum CRP was decreased in EHHD patients suggesting that extended dialysis may decrease

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21

Jayatunga, Dona Pamoda Wajirapanie. "Investigation of selected nutraceuticals to protect against mitochondrial dysfunction: Potential therapeutic role in Alzheimer’s disease." Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2020. https://ro.ecu.edu.au/theses/2368.

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Alzheimer’s disease (AD) is a devastating neurodegenerative disorder that affects approximately 60-80% of all clinically diagnosed dementia cases worldwide. It is the second major cause of death in Australia. The progressive nature of the disease is characterized by cognitive deficits that worsen over time, usually leading to death within about a decade from their first manifestation. The AD brain is classically characterized by extracellular deposition of amyloid-β (Aβ) protein aggregates, as senile plaques, and intracellular neurofibrillary tangles (NFTs), composed of hyper-phosphorylated fo

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22

Robineau-Charette, Pascale. "Function and Dysfunction of Fibrinogen-Like Protein 2 in Reproductive Success and Preeclampsia." Thesis, Université d'Ottawa / University of Ottawa, 2021. http://hdl.handle.net/10393/41999.

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Fibrinogen-like protein 2 (FGL2) is a known immunomodulator and prothrombinase, expressed by several subsets of immune cells. This thesis explores its potential role during the establishment of pregnancy, in mice, as well as in trophoblast function and in an immune-mediated subtype of preeclampsia (PE), in humans. We first noticed a marked subfertility in Fgl2 knockout (ko) and Fgl2 overexpressing (tg) colonies, where litters were fewer and smaller. To explain this, we mapped spatiotemporal patterns of FGL2 expression in the female reproductive tract and through the estrous cycle. FGL2 is expr

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23

King, Billy Ellis. "T-cell Dysfunction by HCV Core Protein Involves PD-1/PD-L1 Signaling." Digital Commons @ East Tennessee State University, 2007. https://dc.etsu.edu/etd/2082.

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In 1989 the hepatitis C virus was identified as a significant cause of post-transfusion hepatitis. Nearly two decades later there is still no vaccine, inadequate treatment options, and limited understanding of how the virus establishes chronicity in the majority of the people it infects. Recent reports suggest that the interaction of a negative co-stimulatory pathway mediated by PD-1 and PDL-1 is associated with persistent viral infection. The role, if any, that PD-1/PDL-1 has in HCV infection is unknown. In this study we report that PD-1 is upregulated in T-cells from persons with chronic HCV

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24

Sargeant, Amy. "Semiotics of disillusionment: Protesting and Reframing Australia's political spectacle through détournement." Thesis, Queensland University of Technology, 2020. https://eprints.qut.edu.au/206454/1/Amy_Sargeant_Thesis.pdf.

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This practice-led research project explores and expresses my disillusionment with the dysfunctions of the political establishment in Australia. This is achieved by reframing the visual elements of political spectacle through the installation of video, audio and sculpture, deployed in public and gallery settings. The research is enacted through a Rancièrian lens and uses a practice-led methodology, deploying the Situationist method of détournement to de-stabilise points of symbolic reference appropriated from Australian politics.

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25

Meier, Shelby. "PATHOLOGICAL TAU AS A CAUSE, AND CONSEQUENCE, OF CELLULAR DYSFUNCTION." UKnowledge, 2019. https://uknowledge.uky.edu/physiology_etds/44.

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Tauopathies are a group of neurodegenerative diseases characterized by the abnormal deposition of the protein tau, a microtubule stabilizing protein. Under normal physiological conditions tau is a highly soluble protein that is not prone to aggregation. In disease states alterations to tau lead to enhanced fibril formation and aggregation, eventually forming neurofibrillary tangles (NFTs). The exact cause for NFT deposition is unknown, but increased post-translational modifications and mutations to the tau gene can increase tangle formation. Tauopathic brains are stuck in a detrimental cycle,

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26

Brain, Kirsty Lianne. "Antioxidants protect against fetal growth restriction and offspring cardiovascular dysfunction in adulthood following ovine hypoxic pregnancy." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708698.

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27

Akbar, Naveed. "Systemic cytokine expression and endothelial dysfunction : insights from innate immune models of protein phosphorylation." Thesis, University of Dundee, 2014. https://discovery.dundee.ac.uk/en/studentTheses/ad1500e7-9160-4765-8a8e-b26fb94ce1e5.

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Cardiovascular diseases (CVD) are united in pathology by atherosclerosis; signal transduction is essential in this process for the expression of cell adhesion molecules early in the disease, capturing, tethering and transmigrating monocytes into the sub-endothelial space. The local recruitment of inflammatory cells and release of pro-inflammatory mediators induces endothelial dysfunction, an early functional abnormality in CVD. Plasma cytokines have been used to stratify CVD risk in humans. Studies have shown associations between pro-inflammatory tumour necrosis factor (TNF) and interleukin-6

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28

Aktar, Rubina. "Multiple roles for the extracelllular matrix protein Tenascin-X in nerve gut function." Thesis, Queen Mary, University of London, 2016. http://qmro.qmul.ac.uk/xmlui/handle/123456789/18406.

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Tenascin X (TNX) is a matricellular protein involved in regulating cellular functions by interacting with other extracellular matrix (ECM) proteins within the cell matrix and has anti-adhesive properties evidenced in tumours and wound healing. TNX is the only member of the tenascin family that is lost in Joint Hypermobility Syndrome (JHS) and exerts a crucial architectural function. Of importance, TNX deficient and JHS patients have gastrointestinal (GI) dysfunction. Despite this association no study has described the role of TNX in the GI tract. Thus, the aim of this thesis was to characteris

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Wang, Yiqun. "Berberine as a potential therapeutic agent for treating vascular dysfunction in diabetes : targeting AMP-activated protein kinase /." Click to view the E-thesis via HKUTO, 2010. http://sunzi.lib.hku.hk/hkuto/record/B43703616.

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30

Ting, Jonathan T. "Molecular mechanisms of synapse dysfunction : modeling neurological disease by viral-mediated protein overexpression in mammalian CNS neurons /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/10671.

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31

Majkova, Zuzana. "POLYCHLORINATED BIPHENYL-INDUCED ENDOTHELIAL CELL DYSFUNCTION AND ITS MODULATION BY DIETARY LIPIDS." UKnowledge, 2010. http://uknowledge.uky.edu/gradschool_diss/24.

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Cardiovascular diseases are the number one cause of death in Western societies. Endothelial dysfunction is an early event in the pathology of atherosclerosis, which is an underlying cause in the majority of cardiovascular events. Exposure to persistent environmental pollutants, such as polychlorinated biphenyls (PCBs), is a risk factor for the development of atherosclerosis. First, we tested a hypothesis that coplanar PCBs, dioxin-like chemicals with affinity for aryl hydrocarbon receptor (AhR), can stimulate up-regulation of monocyte chemoattractant protein-1 (MCP-1), an endothelium-derived c

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32

Mastro, Laurel M. "THE EFFECT OF PITUITARY PARS INTERMEDIA DYSFUNCTION ON PROTEIN METABOLISM AND INSULIN SENSITIVITY IN AGED HORSES." UKnowledge, 2013. http://uknowledge.uky.edu/animalsci_etds/31.

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Equine pituitary pars intermedia dysfunction (PPID) typically occurs in horses older than 15 years of age and is characterized by hair coat abnormalities, muscle atrophy and decreased insulin sensitivity. The first objective of this research was to compare the rate of whole body protein metabolism and relative abundance of key factors in the signaling pathways associated with muscle protein synthesis and protein breakdown in response to feeding in Control and PPID horses. No differences (P > 0.05) were seen between the PPID and Control groups in whole-body protein metabolism or post-prandial a

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33

Bailey, Joanne Louise. "Using Hi-Spots to investigate in vitro network dysfunction in Cysteine String Protein α knockout mice". Thesis, University of Southampton, 2010. https://eprints.soton.ac.uk/181815/.

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Hi-Spot are highly re-aggregated neural cultures grown on PTFE membrane at the liquidair interface. The Hi-Spot protocol was developed by scientists at Capsant Neurotechnologies using embryonic neural tissue. We characterised Hi-Spots made using existing protocols to confirm they represented a maturing neural network with molecular, cellular and functional signatures. We have additionally modified existing protocols to allow use of postnatal tissue as the source for dissociation and re-aggregation. Hi-Spots made from postnatal day zero (P0) rats self organised into a complex 3D tissue-like str

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34

Ong, Kai Li. "SNFing Glucose to PASs Mitochondrial Dysfunction: The Role of Two Sensory Protein Kinases in Metabolic Diseases." BYU ScholarsArchive, 2019. https://scholarsarchive.byu.edu/etd/8587.

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Mitochondria is no longer viewed as merely a powerhouse of the cell. It is now apparentthat mitochondria play a central role in signaling, maintaining cellular homeostasis and cell fate.Mitochondrial dysfunction has been linked to many human diseases caused by cellular metabolicderegulation, such as obesity, diabetes, neurodegenerative disease, cardiovascular disease andcancer. Eukaryotic organisms have evolved an efficient way in sensing, communicating andresponding to cellular stress and regulating mitochondrial activity correspondingly through acomplex network of intercommunicating protein

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35

Boon, Ai Ching. "Physiological Effects of Bilirubin: Protection from Protein Oxidation, Kidney Dysfunction and Regulation of Hepatic Lipid Metabolism." Thesis, Griffith University, 2015. http://hdl.handle.net/10072/367250.

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Clinical evidence indicates that hyperbilirubinaemic individuals with Gilbert’s syndrome (GS) are at reduced risk of developing cardiovascular and chronic kidney disease. This thesis consists of five manuscripts which review and explore various mechanisms whereby unconjugated bilirubin (UCB) may prevent cardiovascular disease (CVD) and chronic kidney disease (CKD). The first study of this thesis followed and extended upon the candidate’s Master of Medical Research program. Forty-four age, gender and body mass index matched Gilbert’s syndrome (GS) and healthy controls were recruited and blood w

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Argenti, Marta. "The role of mitochondrial dysfunction in Huntington's disease: pathogenesis and its relation with striatal Rhes protein." Doctoral thesis, Università degli studi di Padova, 2014. http://hdl.handle.net/11577/3423554.

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Huntington's disease (HD) in a fatal and hereditary neurodegenerative disorder. It is caused by a single mutation within the gene which codes for huntingtin protein (Htt). Mutant Htt (mHtt) bears an abnormally long polyglutamine expansion at its N-terminus that makes the protein cytotoxic and prone to aggregation. It is known that mHtt can negatively affect several different cell processes and mitochondrial function appears to be particularly injured. What is still under debate is whether mitochondrial dysfunction represents just an epiphenomenon of the cellular degeneration or it has an actua

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Rida, Ahmad. "Biochemical and structural characterization of Selenoprotein N and study of his dysfunction in pancreatic tissue." Electronic Thesis or Diss., Strasbourg, 2023. http://www.theses.fr/2023STRAJ128.

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Chez l'homme, des mutations dans le gène SELENON, codant pour la sélénoprotéine N (SelenoN), provoquent un groupe de maladies musculaires héréditaires appelés myopathies liées à SELENON. Les mécanismes pathologiques à l'origine de ces myopathies sont mal compris, car la fonction catalytique de SelenoN reste incomprise. L'utilisation de modèles animaux a révélé l'importance de SelenoN dans le développement, la maintenance et la régénération des muscles. En outre, il a été démontré que SelenoN joue un rôle important dans le contrôle du stress oxydatif dans le réticulum endoplasmique et le mainti

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Wang, Yiqun, and 王逸群. "Berberine as a potential therapeutic agent for treating vascular dysfunction in diabetes: targeting AMP-activated protein kinase." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B43703616.

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Wagey-Radjawane, Theophilia Ravenska Elizabeth. "A role of protein kinase C (PKC) and phosphatidylinositol-3-kinase (PI 3-K) in motoneuron dysfunction." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ61192.pdf.

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Singh, Neha. "Nos1-Adaptor Protein Dysfunction in the Nucleus Tractus Solitarii Contributes to the Neurogenic Heart Damage and Qt Interval Prolongation." Diss., North Dakota State University, 2015. https://hdl.handle.net/10365/27303.

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Variants of the Nitric Oxide Synthase 1 Adaptor Protein (NOS1AP) locus are strongly related to QT interval prolongation and sudden cardiac death (SCD) in human. Neurogenic cardiac damage due to subarachnoid hemorrhage, stroke, epilepsy and myocardial infarction is known to contribute to sudden death in most cases. Our aim was to study the role of NOS1AP in the neurogenic cardiac damage by silencing NOS1AP expression in the Nucleus Tractus Solitarii (NTS) area of the brainstem using lentiviral vector-mediated NOS1AP shRNA (Lv-NOS1AP-shRNA). Real time PCR data showed NOS1AP mRNA levels were expr

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Ghirardini, E. "THE INTERACTION BETWEEN MUTANT PRION PROTEIN AND GLUTAMATE RECEPTORS: A NOVEL MECHANISM FOR NEURONAL DYSFUNCTION IN GENETIC PRION DISEASES." Doctoral thesis, Università degli Studi di Milano, 2017. http://hdl.handle.net/2434/468275.

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Genetic prion diseases are rare, invariably fatal neurodegenerative disorders linked to mutations in the PRNP gene encoding the prion protein (PrP). PRNP mutations favor the conformational conversion of PrP into a pathogenic, misfolded isoform that accumulates in the central nervous system of affected individuals and kills neurons through an unknown mechanism. Evidence is emerging that neuronal loss in inherited prion diseases is preceded and possibly caused by synaptic dysfunctions. However, the ultimate link between synaptic dysfunction and neurodegeneration is yet to be found. We previous

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Wang, Bingjie. "Novel function of human beta-defensin 2 : protecting epidermal barrier against pathogenic proteases." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28756.

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Atopic Dermatitis (AD) is a common chronic relapsing inflammatory skin disease affecting 15 - 20% of children and 2 - 10% of adults worldwide, with significant morbidity. A hallmark of AD is disruption of the critical barrier function of upper epidermal layers, causatively linked to environmental stimuli, genetics and infections. Another typical feature of AD is skin infections, especially from Staphylococcus aureus (S. aureus), which closely relates with the disease severity. Although not a normal flora, S. aureus is found on 75-100% of AD lesions (< 30% on healthy skin). S. aureus secrete a

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Roman, Andrei. "Tau protein aggregation and α-synuclein dysfunction : development of new in vitro and in vivo models to study neurodegenerative diseases". Thesis, Aix-Marseille, 2018. http://www.theses.fr/2018AIXM0281.

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Les signatures histopathologiques de principales maladies neurodégénératives - maladie d'Alzheimer et la maladie de Parkinson - sont les enchevêtrements neurofibrillaires formés par la protéine tau et les corps de Lewy, formés par l'α-synucleine agrégée. Les mécanismes précis du repliement et de l'agrégation de ces protéines, pour la protéine tau comme pour l'α-synucleine, ne sont pas totalement compris à ce jour. Ici, nous nous sommes intéressés à cette question en utilisant des modèles in vitro et in vivo. En étudiant l'agrégation tau in vitro, nous avons mis en évidence un nouvel auto- asse

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Mohan, Megha. "Role of VPS35 in the pathogenesis of Parkinson's disease." Thesis, Griffith University, 2017. http://hdl.handle.net/10072/370642.

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Parkinson’s disease (PD) is a heterogeneous and complex neurodegenerative disorder whose aetiology is not fully understood. Studying familial Parkinson’s disease has identified several mutations that cause the disease and investigating the functions of these genes has given us clues to the cellular mechanisms that underlie the neurodegenerative phenotype in the patients. A clear understanding of these cellular mechanisms is necessary to halt disease progression. Next generation sequencing of a Swiss kindred with autosomal dominant Parkinson’s disease has identified a causative D620N mutation i

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Fullick, Julia. "You Scratch My Back and I'll Scratch Yours: Mentor-Perceived Costs and Benefits and the Functions They Provide Their Proteges." Master's thesis, University of Central Florida, 2008. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/2278.

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Mentoring relationships can have both costs and benefits for mentors and their proteges. The present research examined the degree to which mentors' perceived costs and benefits affect the functional and dysfunctional mentoring they provide to their proteges. Additionally, I investigated whether mentor-perceived costs and benefits were associated with the mentors' own goal orientation and the goal orientation of their proteges. Data were collected from 86 proteges and their current supervisory mentors. Consistent with expectations, when mentors reported greater costs of embarrassment associated

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Davies, R. J. "Dysfunctional response to transforming growth factor-beta contribute to the development of familial pulmonary arterial hypertension due to mutations in bone morphogenetic protein type II receptor." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598337.

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TGF-β<sub>1</sub> significantly inhibited the growth of human and mouse control cells. Cells harbouring dysfunctional BMPR-11 signalling were resistant to this growth inhibition. Mutant BMPR-11 cells had reduced BMP4 induced Smad 1/5 phosphorylation, reduced transcription of the BRE-luciferase reporter as well as reduced induction of inhibitors of DNA binding gene (Id1, 2 and 4) transcription. However, there was no difference in the level of activation of the TGF-β pathway, either at second messenger or transcriptional level, between control and mutant PASMCs to account for the loss of the gro

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Brown, Josephine M. B. S. "Intranasal carnosine protects against alpha-synuclein accumulation in the substantia nigra and motor dysfunction in the Thy1-aSyn mouse model of Parkinson’s disease." University of Cincinnati / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1573571387865684.

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Singh, Neha. "Nitric Oxide Synthase 1 Adaptor Protein Dysfunction in the Nucleus Tractus Solitarii Contributes to the Neurogenic Cardiac Damage and QT Interval Prolongation." Diss., North Dakota State University, 2015. http://hdl.handle.net/10365/24790.

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Salazar, Vázquez Lilian Shadai. "How protein misfolding can lead to cellular dysfunction and disease : the case of islet amyloid polypeptide involved in type 2 diabetes mellitus." Thesis, Sorbonne université, 2019. https://accesdistant.sorbonne-universite.fr/login?url=http://theses-intra.upmc.fr/modules/resources/download/theses/2019SORUS371.pdf.

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Pour avoir une fonction biologique, une protéine se replie dans une structure spécifique. La cellule contrôle le repliement correct des protéines et dispose de mécanismes pour détecter et éliminer les protéines mal repliées. Néanmoins, certaines protéines évitent ce processus de contrôle. Les protéines amyloïdes sont des protéines mal repliées qui forment un type caractéristique de fibrilles amyloïdes allongées; en fonction de la séquence protéique et du site de dépôt de l'amyloïde, ils sont liés à différentes maladies. Le polypeptide amyloïde d'îlot (IAPP), un peptide de 37 acides aminés copr

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Wang, Xiao suo. "A Novel ELISA to Detect Methionine Sulfoxide−Containing Apolipoprotein A−I." University of Sydney, 2009. http://hdl.handle.net/2123/5423.

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Doctor of Philosophy(PhD)<br>Atherosclerosis manifests a state of increased oxidative stress characterized by comparable lipid and protein oxidation in the affected arterial wall. While oxidative modification of low density lipoprotein (LDL) has been extensively studied, increasing attention has been focused recently on oxidation of high-density lipoproteins (HDL) and its functional consequences in relation to atherosclerosis. Oxidative modification is thought to generate “dysfunctional” HDL that has lost anti-atherosclerotic activities, including the ability to remove cholesterol from lipid-l

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