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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

Serum amyloid A protein (SAA) in healthy and infected individuals /

Lannergård, Anders, January 2005 (has links)
Diss. (sammanfattning) Uppsala : Uppsala universitet, 2005. / Härtill 5 uppsatser.
2

Influence de l'environnement alvéolaire sur les monocytes/macrophages au cours du Syndrome de Détresse Respiratoire Aigüe : rôle sur la réparation alvéolaire / Influence of the alveolar environment on monocytes/macrophages during the Acute Respiratory Distress Syndrome : role on alveolar repair

Garnier, Marc 28 November 2016 (has links)
Le Syndrome de Détresse Respiratoire Aiguë (SDRA) est la forme la plus sévère d’agression alvéolaire aiguë. Il estcaractérisé par un dommage alvéolaire diffus, suivi d’une phase de réparation nécessaire à la guérison. Bien queles monocytes/macrophages soient des acteurs incontournables de la pathogénie et de la résolution du SDRA, leurpolarisation et leur rôle dans la réparation alvéolaire restent mal connus chez l’Homme. L’hypothèse défendue parcette thèse est que l’environnement alvéolaire module la différenciation et la polarisation desmonocytes/macrophages au cours du SDRA, et que les macrophages alvéolaires ainsi polarisés participentactivement à la réparation et à sa régulation. Les principaux résultats de nos travaux ont permis d’établir que : 1)l’environnement alvéolaire de SDRA inhibe la différenciation des monocytes en fibrocytes (précurseursmésenchymateux associés à la fibroprolifération et à pronostic péjoratif). L’inhibition est majoritairement due à laSerum Amyloid protein P (SAP), provenant en partie du relargage de ses stocks matriciels pulmonaires à la faveurde la lésion alvéolaire ; 2) l’environnement alvéolaire de SDRA induit une polarisation anti-inflammatoire desmacrophages se rapprochant de la polarisation induite in vitro par l’IL-10 ; 3) les macrophages anti-inflammatoirespolarisés par le lavage broncho-alvéolaire (LBA) de patients SDRA favorisent la réparation alvéolaire épithéliale viala production polarisation-dépendante d’Hepatocyte Growth Factor (HGF). Cette production macrophagique d’HGFest amplifiée via une boucle autocrine PTGS2/PGE2 chez l’Homme ; 4) ces résultats semblent étayés par lesdonnées obtenues sur une cohorte clinique qui montrent que les concentrations de sCD163 (marqueur depolarisation anti-inflammatoire) et d’HGF rapportées au nombre de macrophages alvéolaires sont plus élevéeschez les patients survivants que chez les patients décédés de SDRA. L’ensemble de nos travaux démontrent pour lapremière fois chez l’Homme le rôle bénéfique de l’environnement alvéolaire sur les monocytes/macrophages,d’une part en inhibant leur différenciation en fibrocytes contribuant ainsi à limiter la fibroprolifération pulmonaire,et d’autre part en induisant un phénotype macrophagique anti-inflammatoire, contribuant à limiter l’inflammationengendrée par la lésion alvéolaire initiale et favorisant la réparation épithéliale via la production d’HGF. Lesdonnées physiopathologiques obtenues pourraient permettre d’envisager la reprogrammation anti-inflammatoiredes macrophages comme une cible thérapeutique du SDRA en cas d’excès d’inflammation ou de fibro-proliférationavec réparation aberrante. / Acute Respiratory Distress Syndrome (ARDS) is the most severe form of acute lung injury. ARDS is characterized bydiffuse alveolar damage followed by a phase of alveolar repair necessary to recovery. Althoughmonocytes/macrophages are key actors of pathogenicity and resolution of ARDS, little is known about theirpolarization and role on alveolar repair during human ARDS. The hypothesis of our studies was that ARDS alveolarenvironment modulates differentiation and polarization of monocytes and macrophages, and that polarizedmacrophages are involved in alveolar repair and its regulation. The main results of our work have shown that: 1)ARDS alveolar environment inhibited monocytes differentiation into fibrocytes (mesenchymal progenitorsassociated with fibroprolifération and a poor prognosis), mainly through its Serum Amyloid P (SAP) content,originating, at least in part, from the release of SAP associated with lung connective tissue during ARDS; 2) ARDSalveolar environment drove an anti-inflammatory macrophage polarization, close to that induced by IL-10 in vitro;3) anti-inflammatory macrophages polarized by broncho-alveolar lavage (BAL) from ARDS patients favored alveolarepithelial repair through a polarization-dependent production of Hepatocyte Growth Factor (HGF). This HGFproduction is amplified by an autocrine PTGS2/PGE2 dependent loop in human macrophages; 4) these results mayhave clinical relevance, since sCD163 (a marker of anti-inflammatory polarization) and HGF concentrations,expressed relatively to BAL macrophage count, were higher in ARDS survivors than non-survivors. Taken together,our works demonstrate for the first time the beneficial role of the ARDS alveolar environment onmonocytes/macrophages, inhibiting their differentiation into fibrocytes, thus limiting excessive lungfibroproliferation, and inducing an anti-inflammatory macrophage polarization, thus limiting the inflammationgenerated by the initial alveolar damage and favoring epithelial repair through HGF production. The datapresented in this thesis may allow considering anti-inflammatory macrophage repolarization as a potential newtherapeutic target of ARDS with excessive inflammation or fibro-proliferation with aberrant repair.
3

Serum Amyloid P Component and Systemic Fungal Infection: Does It Protect the Host or Is It a Trojan Horse?

Klotz, Stephen A., Sobonya, Richard E., Lipke, Peter N., Garcia-Sherman, Melissa C. 05 1900 (has links)
It is a striking observation that tissue of patients invaded by the deep mycoses often lacks evidence of an inflammatory response. This lack of host response is often attributed to neutropenia secondary to chemotherapy. However, systematic studies do not support this simplistic explanation. However, invasive fungal lesions are characterized by abundant fungal functional amyloid, which in turn is bound by serum amyloid P component (SAP). We postulate that SAP is important in the local immune response in invasive fungal infections. The interaction between fungal functional amyloid, SAP, and the immune response in deep mycoses is discussed.
4

A Logistic Normal Mixture Model for Compositions with Essential Zeros

Bear, John Stanley, Bear, John Stanley January 2016 (has links)
Compositions are vectors of nonnegative numbers that sum to a constant, usually one or 100%. They arise in a wide array of fields: geological sampling, budgets,fat/protein/carbohydrate in foods, percentage of the vote acquired by each political party, and more. The usual candidate distributions for modeling compositions -- the Dirichlet and the logistic normal distribution -- have density zero if any component is zero. While statistical methods have been developed for "rounded" zeros, zeros stemming from values below a detection level, and zeros arising from count data, there remain problems with essential zeros, i.e. cases in continuous compositions where a component is truly absent. We develop a model for compositions with essential zeros based on an approach by Aitchison and Kay (2003). It uses a mixture of additive logistic normal distributions of different dimension, related by common parameters. With the requirement of an additional constraint, we develop a likelihood and methods estimating parameters for location and dispersion. We also develop a permutation test for a two-group comparison, and demonstrate the model and test using data from a diabetes study. These results provide the first use of the additive logistic normal distribution formodeling and testing compositional data in the presence of essential zeros.
5

Heparan Sulfate Dependent Mechanisms of Amyloidosis

Noborn, Fredrik January 2012 (has links)
A common theme in amyloid disorders is the deposition of disease-specific protein aggregates in tissues. Amyloid proteins bind to heparan sulfate (HS), a sulfated glycosaminoglycan, and HS has been found to promote the aggregation process. The present work relates to HS mediated mechanisms of amyloidosis, particularly transthyretin (TTR) amyloidosis, AA-amyloidosis and Alzheimer’s disease (AD). TTR is a transport protein present in the blood and cerebrospinal fluid, which under unclear circumstances can deposit as amyloid in the myocardium of elderly individuals. Examination of cardiac tissue from a 70 year old patient with reported cardiomyopathy reveald co-deposition of TTR amyloid and HS. Studies revealed that HS promotes TTR fibrillization through interaction with a basic motif in the protein. Empolyment of a cell model demonstrated that cell surface HS mediates internalization of TTR, an effect likely facilitated by HS-binding to the basic motif on TTR. Collectively, HS-TTR interactions at the cell surface may have dual outcomes, resulting in either fibrillization or internalization, respectively. During inflammatory conditions, serum amyloid A (SAA), an acute-phase protein associated with the high-density lipoprotein (HDL), can assemble into insoluble amyloid fibrils, causing AA-amyloidosis. We found that HS structures exceeding 12-14 sugar units in length separates SAA from HDL and induces subsequent aggregation of the polypeptide. Our result proposes a novel role for HS in AA-amyloidosis in which a critical length of HS is required for separation of SAA from HDL. Late-onset AD patients show reduced ability to clear cerebral amyloid-β (Aβ) aggregates, a pathological hallmark of the disease. Althought the pathway of Aβ clearance is still unclear, several cell-surface receptors are implicated in Aβ internalization. We found that ApoE facilitated Aβ uptake through interactions with HS-proteoglycans and low-density lipoprotein receptor-related protein 1. The ApoE interaction with Aβ likely promotes Aβ clearance in the brain, but, if unbalanced, may contribute to the pathology of AD.     These findings are in accord with the concept of HS as a promoter of amyloid protein aggregation, but also point to more complex relationship.
6

A Brief Elevation of Serum Amyloid A is Sufficient to Increase Atherosclerosis

Thompson, Joel C 01 January 2014 (has links)
Cardiovascular disease is now the leading cause of death worldwide. Serum amyloid A (SAA), a positive acute phase reactant, along with C-reactive protein is used clinically as a marker of cardiovascular disease risk. However, recent data has shed light on a possible causal role of SAA in the development of atherosclerosis, the most pervasive form of cardiovascular disease. Several inflammatory diseases such as diabetes and obesity are known to confer increased risk of developing cardiovascular disease. Individuals with these diseases all have modest but persistent elevation of SAA. To determine if SAA caused the development of atherosclerosis, apoe-/-chow fed mice were injected with either an adenoviral vector expressing human SAA1 (ad-hSAA1), a null adenoviral vector (ad-Null) or saline. Human SAA levels rapidly increased, albeit briefly then returned to baseline within 14 days in mice that received ad-hSAA1. After 16 weeks, mice that received ad-hSAA1 had significantly increased atherosclerosis compared to controls on the aortic intimal surface (p<0.0001), aortic sinus (p<0.05) and the brachiocephalic artery (p<0.05). According to the “response to retention” hypothesis; lipoprotein retention by vascular wall proteoglycans is a key initiating event in the development of atherosclerosis. We previously reported that SAA-stimulated vascular smooth muscle cells expressed biglycan with increased glycosaminoglycan chain length and increased binding affinity for low density lipoprotein. To further test the role of biglycan on the development of atherosclerosis we generated biglycan transgenic mice. These mice were crossed to the ldlr-/- mouse on a C57BL/6 background and fed a pro-atherogenic western diet for 12 weeks. There was a significant increase in atherosclerotic lesion area on the aortic intimal surface (p<0.05) and the aortic sinus (p<0.006), as well as a significant correlation between vascular biglycan content and aortic sinus atherosclerotic lesion area (p<0.0001). These data demonstrate that transiently increased SAA resulted in increased atherosclerosis compared to control mice, possibly via increased vascular biglycan content. In support of this we found that biglycan transgenic mice had significantly increased atherosclerosis compared to wildtype controls, likely through increased lipid retention in the vascular wall.
7

Prefibrillar oligomeric Transthyretin mutants : amyloid conformation, toxicity and association with Serum amyloid P component /

Andersson, Karin, January 2005 (has links)
Diss. (sammanfattning) Umeå : Umeå universitet, 2005. / Härtill 4 uppsatser.
8

Tenomodulin, serum amyloid A and the serum amyloid A receptor selenoprotein S : implications for metabolic disease /

Olsson, Maja, January 2010 (has links)
Diss. (sammanfattning) Göteborg : Göteborgs universitet, 2010. / Härtill 4 uppsatser.
9

Equine Septic Arthritis and Serum Amyloid A

Ludwig, Elsa Karen 07 July 2016 (has links)
Bacterial infection within a joint, septic arthritis, is a serious condition in horses that can lead to long-term joint disease if the infection is not resolved quickly. Equine septic arthritis is diagnosed primarily based on clinical signs and synovial fluid cytology. Septic synovial fluid is characterized by significant elevations in total protein (TP) and total nucleated cell count (TNCC). However, in some cases it can be difficult to distinguish between septic arthritis and non-septic joint inflammation (synovitis) based on clinical signs and synovial fluid cytology alone. A rapid assay to help confirm septic arthritis would be advantageous. A new assay to quantify the major equine acute phase protein, serum amyloid A (SAA) may fulfill this need. Serum amyloid A increases in the body in response to injury, infection, and inflammation and shows promise as a useful tool in confirming a diagnosis of sepsis, as inflammation causes mild increases in SAA and infection causes marked elevations. In our study, serial serum and synovial fluid samples were collected from horses with experimental models of synovitis and septic arthritis, synovial fluid cytology was performed, and serum and synovial fluid SAA were quantified. Synovial fluid TNCC and TP concentrations increased significantly following induction of both models. Serum and synovial fluid SAA concentrations remained normal in synovitis horses and increased significantly in septic arthritis horses. Any elevation in serum or synovial fluid SAA above normal values may be supportive of synovial sepsis since synovial inflammation alone did not result in SAA elevations in our model. / Master of Science
10

Effect of arthroscopic lavage and repeated through-and-through joint lavage on systemic and synovial serum amyloid A concentrations; as well as total protein concentrations, nucleated cell count and percentage of neutrophils in synovial fluid from healthy equine joints

2015 June 1900 (has links)
This research evaluated serum amyloid A (SAA) concentration in synovial fluid of healthy horses as a potential marker for use in the diagnosis and monitoring of horses with septic arthritis. The first study evaluated the effect of arthroscopic lavage of healthy joints on concentrations of systemic and synovial SAA; as well as total protein concentration, nucleated cell count and percentage of neutrophils in synovial fluid. The second study, evaluated the effect of repeated through-and-through joint lavage on SAA in systemic blood and SAA, total protein, nucleated cell count and percentage of neutrophils in synovial fluid from healthy joints. In the first study, middle carpal joints of 6 horses were randomly assigned to one of the following treatments 1) arthrocentesis (controls) or 2) arthroscopic lavage. A washout period of 30 days was allowed in between treatments. Synovial fluid and blood samples were collected at 0, 24, 48, 72, 96 and 120 h. Measurements included SAA in blood and synovial fluid, and total protein, nucleated cell count and percentages of neutrophils in synovial fluid. In the second study, one tarsocrural joint was randomly assigned to receive repeated through-and-through joint lavage at 0, 48 and 96 h in 6 horses. Synovial fluid and blood samples were collected at 0, 24, 48, 72, 96 and 120 h. Measurements included SAA in blood and synovial fluid, and total protein, nucleated cell count and percentages of neutrophils in synovial fluid. For this study, synovial fluid samples collected at time 0 were considered as control values. After arthroscopic lavage and repeated through-and-through joint lavage, systemic and synovial SAA did not increase from baseline values (except for systemic SAA at 24h after arthroscopic lavage and in controls). Total protein values were significantly increased at all time points after arthroscopic and through-and-through joint lavages (except at 96h on both lavage procedures) but not in controls. With both lavage procedures, nucleated cell count significantly increased from baseline values at all time points (except at 96h after through-and-through joint lavage). Percentage of neutrophils was significantly increased after arthroscopic lavage at all time points and only at 24h in controls; however, the percentages of neutrophils were not significantly increased after repeated through-and-through joint lavage. Synovial SAA was not affected by arthroscopic or repeated through-and-through joint lavage; however, synovial total protein and nucleated cell counts were significantly increased. Synovial SAA may be a valuable inflammatory marker that is not affected by procedures as arthroscopic or repeated through-and-through joint lavage in horses. Further validation of synovial SAA as a marker for evaluating the progression of septic joints while treatment is installed is warranted.

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