subject:( inflammation)

1. Millet, Patrick. INTERDEPENDENT REGULATION OF METABOLISM AND INFLAMMATION IN HUMAN MONOCYTES.

Degree: 2015, Wake Forest University

► Sepsis is serious medical condition which kills millions of people worldwide each year. In the United States, severe sepsis has a mortality rate of 20-30%,… (more)

Subjects/Keywords: Inflammation

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APA (6^th Edition):

Millet, P. (2015). INTERDEPENDENT REGULATION OF METABOLISM AND INFLAMMATION IN HUMAN MONOCYTES. (Thesis). Wake Forest University. Retrieved from http://hdl.handle.net/10339/57421

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):

Millet, Patrick. “INTERDEPENDENT REGULATION OF METABOLISM AND INFLAMMATION IN HUMAN MONOCYTES.” 2015. Thesis, Wake Forest University. Accessed April 13, 2021. http://hdl.handle.net/10339/57421.

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

MLA Handbook (7^th Edition):

Millet, Patrick. “INTERDEPENDENT REGULATION OF METABOLISM AND INFLAMMATION IN HUMAN MONOCYTES.” 2015. Web. 13 Apr 2021.

Vancouver:

Millet P. INTERDEPENDENT REGULATION OF METABOLISM AND INFLAMMATION IN HUMAN MONOCYTES. [Internet] [Thesis]. Wake Forest University; 2015. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10339/57421.

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

Council of Science Editors:

Millet P. INTERDEPENDENT REGULATION OF METABOLISM AND INFLAMMATION IN HUMAN MONOCYTES. [Thesis]. Wake Forest University; 2015. Available from: http://hdl.handle.net/10339/57421

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

2. Neyrinck-Leglantier, Déborah. Implication de zonula occludens-1 dans les processus pro-inflammatoires associés à la progression métastatique des cancers broncho-pulmonaires : Involvement of zonula occludens-1 in pro-inflammatory processes associated to metastatic progression of lung cancers.

Degree: Docteur es, Médecine, 2018, Reims

URL: http://www.theses.fr/2018REIMM212

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Zonula occludens 1 (ZO-1) est une protéine sous-membranaire des jonctions serrées impliquée dans l’organisation structurale des cellules épithéliales. Au cours de la progression tumorale, associée… (more)

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Zonula occludens 1 (ZO-1) est une protéine sous-membranaire des jonctions serrées impliquée dans l’organisation structurale des cellules épithéliales. Au cours de la progression tumorale, associée au processus de transition épithélio-mésenchymateuse (TEM), les composants des jonctions intercellulaires sont réorganisés. Notamment, lors de la TEM, la protéine ZO-1 est délocalisée de la membrane vers le cytoplasme et/ou le noyau où elle adopte alors un rôle pro-invasif. Nous avons d’ailleurs montré que ZO-1 cyto-nucléaire régule l’expression de la chimiokine IL-8 dans les cancers broncho-pulmonaires non à petites cellules (CBNPC). Nous nous sommes donc intéressés à l’influence de ZO-1 cyto-nucléaire sur le recrutement des cellules inflammatoires dans les CBNPC. In vitro, le niveau d’expression de ZO-1 module le recrutement de la lignée monocytaire THP-1. Par différentes techniques in vivo, nous avons montré que la surexpression de ZO-1 cyto-nucléaire favorise le recrutement de cellules inflammatoires et immunitaires à des temps précoce et tardif de la réponse immunitaire. En parallèle, la caractérisation de l’infiltrat inflammatoire en fonction de la localisation nucléaire de ZO-1 chez les patients atteints de CBNPC a mis en évidence une corrélation entre l’expression cyto-nucléaire de ZO-1 et la présence de lymphocytes T cytotoxiques CD8+ au sein du microenvironnement tumoral.Ainsi, notre étude révèle un nouveau rôle de la protéine structurale ZO-1. En effet, ZO-1 cyto-nucléaire, associé au processus de TEM, est impliqué dans la mise en place et le développement d’un microenvironnement pro-inflammatoire et/ou pro-immunitairepermissif pour la progression tumorale des CBNPC.

Zonula occludens 1 (ZO-1) is a sub-membrane protein of tight junctions involved in the structural organization of epithelial cells. During tumor progression, associated with the epithelial-mesenchymal transition (EMT) process, intercellular junction components are reorganized. In particular, during EMT, ZO-1 protein is delocalized from the membrane to the cytoplasm and/or the nucleus where it then displays pro-invasive properties. We have shown that ZO-1 cyto-nuclear regulates the expression of chemokine IL-8 in non-small cell lung cancer (NSCLC). We are therefore interested in the influence of cyto-nuclear ZO-1 on the recruitment of inflammatory cells in NSCLC. In vitro, the level of expression of ZO-1 modulates the recruitment of the monocyte-like cell line THP-1. By different in vivo techniques, we have shown that overexpression of cyto-nuclear ZO-1 promotes the recruitment of inflammatory and immune cells at early and late times of the immune response. In parallel, the characterization of the inflammatory infiltrate as a function of the nuclear localization of ZO-1in patients with NSCLC revealed a correlation between the cyto-nuclear expression of ZO-1 and the presence of cytotoxic T lymphocytes CD8+ within the tumor microenvironment.Thus, our study reveals a new role of structural protein ZO-1. Indeed, ZO-1 cyto-nuclear, associated with the…

Advisors/Committee Members: Polette, Myriam (thesis director), Gilles, Christine (thesis director).

Subjects/Keywords: Inflammation; Inflammation; 570

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

APA (6^th Edition):

Neyrinck-Leglantier, D. (2018). Implication de zonula occludens-1 dans les processus pro-inflammatoires associés à la progression métastatique des cancers broncho-pulmonaires : Involvement of zonula occludens-1 in pro-inflammatory processes associated to metastatic progression of lung cancers. (Doctoral Dissertation). Reims. Retrieved from http://www.theses.fr/2018REIMM212

Chicago Manual of Style (16^th Edition):

Neyrinck-Leglantier, Déborah. “Implication de zonula occludens-1 dans les processus pro-inflammatoires associés à la progression métastatique des cancers broncho-pulmonaires : Involvement of zonula occludens-1 in pro-inflammatory processes associated to metastatic progression of lung cancers.” 2018. Doctoral Dissertation, Reims. Accessed April 13, 2021. http://www.theses.fr/2018REIMM212.

MLA Handbook (7^th Edition):

Neyrinck-Leglantier, Déborah. “Implication de zonula occludens-1 dans les processus pro-inflammatoires associés à la progression métastatique des cancers broncho-pulmonaires : Involvement of zonula occludens-1 in pro-inflammatory processes associated to metastatic progression of lung cancers.” 2018. Web. 13 Apr 2021.

Vancouver:

Neyrinck-Leglantier D. Implication de zonula occludens-1 dans les processus pro-inflammatoires associés à la progression métastatique des cancers broncho-pulmonaires : Involvement of zonula occludens-1 in pro-inflammatory processes associated to metastatic progression of lung cancers. [Internet] [Doctoral dissertation]. Reims; 2018. [cited 2021 Apr 13]. Available from: http://www.theses.fr/2018REIMM212.

Council of Science Editors:

Neyrinck-Leglantier D. Implication de zonula occludens-1 dans les processus pro-inflammatoires associés à la progression métastatique des cancers broncho-pulmonaires : Involvement of zonula occludens-1 in pro-inflammatory processes associated to metastatic progression of lung cancers. [Doctoral Dissertation]. Reims; 2018. Available from: http://www.theses.fr/2018REIMM212

3. Santinon, François. Rôle du TNFR2 exprimé à la surface des lymphocytes T régulateurs dans l’inflammation dépendante du TNFα : Role of TNFR2 on Tregs in TNF-α-mediated inflammation.

Degree: Docteur es, Biologie, 2018, Sorbonne Paris Cité

URL: http://www.theses.fr/2018USPCD006

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La polyarthrite rhumatoïde (PR) est une maladie inflammatoire chronique d’étiologie inconnue. L’inflammation présente dans cette pathologie est fortement dépendante de la cytokine pro-inflammatoire qu’est le… (more)

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La polyarthrite rhumatoïde (PR) est une maladie inflammatoire chronique d’étiologie inconnue. L’inflammation présente dans cette pathologie est fortement dépendante de la cytokine pro-inflammatoire qu’est le TNFα. Cette molécule possède deux récepteurs : le TNFR1 et le TNFR2. Le TNFR1 est un récepteur exprimé à la surface de toutes les cellules. L’activation de sa voie de signalisation déclenche la mort cellulaire et elle est souvent associée à des phénomènes inflammatoires. Le TNFR2, quant à lui, est exprimé à la surface des cellules immunitaires, des cellules endothéliales et des cellules neuronales. L’activation de la signalisation du TNFR2 conduit à la survie et à la prolifération cellulaire. Le TNFR2 est de plus, associé à des mécanismes anti-inflammatoires. Les lymphocytes T régulateurs (Treg), cellules clé dans le contrôle de la réponse immunitaire, sont caractérisés par l’expression du facteur de transcription Forkhead box P3 (FoxP3) et sont défectueux chez des patients atteints de PR. Ces cellules expriment les deux récepteurs du TNFα et sont capables d’inhiber l’action des cellules inflammatoires et particulièrement des T effecteurs par différents mécanismes d’immunosuppression. Les Treg exprimant le TNFR2 représentent la population la plus immunosuppressive actuellement recensée. L’objectif de notre travail a été de mieux comprendre le rôle des Treg exprimant le TNFR2 dans le contrôle de l’inflammation dépendante du TNFα. Tout d’abord, nous avons montré que la signalisation TNFα-TNFR2 sur les Treg augmentait le maintien de l’expression de FoxP3 ainsi que la prolifération de ces cellules. L’expression du TNFR2 est en outre liée à une stabilité accrue de ces cellules. Ces résultats peuvent expliquer le rôle important que pourraient jouer les Treg TNFR2+ dans le contrôle de l’inflammation dépendante du TNFα. Afin de confirmer cette hypothèse, nous avons démontré, dans deux modèles expérimentaux d’inflammation dépendants du TNFα (arthrite et psoriasis), que les Treg TNFR2+ jouaient un rôle prépondérant dans le contrôle de l’inflammation. Enfin, des expériences effectuées chez des patients atteints de PR ont mis en évidence que les traitements anti-TNFα conduisaient à une augmentation de la fréquence des Treg TNFR2+ circulants chez des patients répondeurs. En démontrant le rôle prépondérant des Treg TNFR2+ dans la résolution de l’inflammation, ce travail ouvre la voie vers l’élaboration de thérapies ciblant le système TNFα/TNFR plus spécifiques pour le traitement de la PR et d’autres pathologies dépendantes du TNF.

Rheumatoid arthritis (RA) is a chronic inflammatory disease with unknown etiology. In this pathology, inflammation is mainly dependent on the pro-inflammatory cytokine TNFα. This molecule acts through two receptors: TNFR1 and TNFR2. TNFR1 is expressed on almost all cell types. Activation of this pathway mainly leads to cell death and is often associated with pro-inflammatory response. In contrast, TNFR2 is expressed on immune, epithelial and neuronal cells. Activation of TNFR2 signaling triggers…

Advisors/Committee Members: Bessis, Natacha (thesis director), Semerano, Luca (thesis director).

Subjects/Keywords: Inflammation chronique; Chronic inflammation

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

APA (6^th Edition):

Santinon, F. (2018). Rôle du TNFR2 exprimé à la surface des lymphocytes T régulateurs dans l’inflammation dépendante du TNFα : Role of TNFR2 on Tregs in TNF-α-mediated inflammation. (Doctoral Dissertation). Sorbonne Paris Cité. Retrieved from http://www.theses.fr/2018USPCD006

Chicago Manual of Style (16^th Edition):

Santinon, François. “Rôle du TNFR2 exprimé à la surface des lymphocytes T régulateurs dans l’inflammation dépendante du TNFα : Role of TNFR2 on Tregs in TNF-α-mediated inflammation.” 2018. Doctoral Dissertation, Sorbonne Paris Cité. Accessed April 13, 2021. http://www.theses.fr/2018USPCD006.

MLA Handbook (7^th Edition):

Santinon, François. “Rôle du TNFR2 exprimé à la surface des lymphocytes T régulateurs dans l’inflammation dépendante du TNFα : Role of TNFR2 on Tregs in TNF-α-mediated inflammation.” 2018. Web. 13 Apr 2021.

Vancouver:

Santinon F. Rôle du TNFR2 exprimé à la surface des lymphocytes T régulateurs dans l’inflammation dépendante du TNFα : Role of TNFR2 on Tregs in TNF-α-mediated inflammation. [Internet] [Doctoral dissertation]. Sorbonne Paris Cité; 2018. [cited 2021 Apr 13]. Available from: http://www.theses.fr/2018USPCD006.

Council of Science Editors:

Santinon F. Rôle du TNFR2 exprimé à la surface des lymphocytes T régulateurs dans l’inflammation dépendante du TNFα : Role of TNFR2 on Tregs in TNF-α-mediated inflammation. [Doctoral Dissertation]. Sorbonne Paris Cité; 2018. Available from: http://www.theses.fr/2018USPCD006

University of Otago

4. Park, Sun-Jin. RAGE Biology and Inflammation .

Degree: 2011, University of Otago

URL: http://hdl.handle.net/10523/1651

► The receptor for advanced glycation end products (RAGE) is a cell surface signal transduction receptor that amplifies inflammation, principally through the activation of nuclear factor… (more)

▼ The receptor for advanced glycation end products (RAGE) is a cell surface signal transduction receptor that amplifies inflammation, principally through the activation of nuclear factor (NF)-κB. A circulating soluble form of RAGE (sRAGE) acts as a “decoy” receptor to alleviate the pro-inflammatory activity mediated by membrane-bound RAGE (mRAGE)-ligand interaction. N-linked glycosylation of RAGE plays an important role in the regulation of ligand binding. Two sites for N-linked glycosylation, at Asn25 and Asn81, are implicated, one of which is potentially influenced by a naturally occurring polymorphism that substitutes Gly82 with Ser (G82S). The G82S RAGE polymorphic variant is associated with reduced plasma sRAGE levels and enhanced ligand-binding. As a consequence, there is increased pro-inflammatory activity associated with the G82S variant. The overall aims of this study were to establish the effects of the G82S polymorphism on RAGE glycosylation and the consequences for sRAGE production and mRAGE-ligand binding. To compare the glycosylation patterns of the G82S variant of RAGE with that for wild-type (WT) receptor, WT-mRAGE or G82S-mRAGE were produced by transfecting human embryonic kidney 293 (HEK293) cells and the glycosylation patterns of expressed proteins were compared. Enzymatic deglycosylation showed that WT-mRAGE and the G82S-mRAGE are glycosylated to the same extent. Furthermore, various mutant forms of mRAGE (N25Q, N81Q, N25Q+G82S, and N25Q+N81Q) were produced to further investigate the complexity of the RAGE glycosylation patterns. Cell surface biotinylation and flow cytometry analysis was used to establish the sub-cellular distribution of WT and all of the mutant forms of mRAGE. All forms reached the cell surface when expressed by HEK293 cells and African Green Monkey SV40-transfected kidney fibroblast cells (COS-7). Mutagenesis and mass spectrometry analysis showed that Asn25 is always “fully” glycosylated in both WT-mRAGE and G82S-mRAGE. However, Asn81 may or may not be glycosylated in WT-mRAGE, whereas in G82S-mRAGE, Asn81 is always “fully” glycosylated. Combined these data indicate that the G82S polymorphism promotes N-linked glycosylation of Asn81. Subsequently, the effects of the enhanced Asn81 glycosylation were investigated. The production of sRAGE via mRAGE ectodomain shedding and the binding of ligand to WT and the variously glycosylated, mutant forms of mRAGE were investigated. Human embryonic kidney 293 cells were transiently transfected with plasmids containing WT or various mutant forms of mRAGE cDNA. To assess matrix metalloproteinase (MMP)-induced mRAGE shedding, surface-expressed mRAGE was biotinylated and transfected cells were treated with potential “shedding inducers” - 4-aminophenylmercuric acetate (APMA) or phorbol 12-myristate 13-acetate (PMA). Levels and component species of mRAGE remaining on the cell surface and of sRAGE released into the cell culture medium were compared by western blot analysis. The data show that reduced amounts of sRAGE were released from transfected… Advisors/Committee Members: Hessian, Paul (advisor).

Subjects/Keywords: Inflammation; RAGE

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

APA (6^th Edition):

Park, S. (2011). RAGE Biology and Inflammation . (Doctoral Dissertation). University of Otago. Retrieved from http://hdl.handle.net/10523/1651

Chicago Manual of Style (16^th Edition):

Park, Sun-Jin. “RAGE Biology and Inflammation .” 2011. Doctoral Dissertation, University of Otago. Accessed April 13, 2021. http://hdl.handle.net/10523/1651.

MLA Handbook (7^th Edition):

Park, Sun-Jin. “RAGE Biology and Inflammation .” 2011. Web. 13 Apr 2021.

Vancouver:

Park S. RAGE Biology and Inflammation . [Internet] [Doctoral dissertation]. University of Otago; 2011. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10523/1651.

Council of Science Editors:

Park S. RAGE Biology and Inflammation . [Doctoral Dissertation]. University of Otago; 2011. Available from: http://hdl.handle.net/10523/1651

Tulane University

5. Sriyotha, Phanuwat. Ethanol-mediated dysregulation of cytokines and human anti-microbial peptide cathelicidin.

Degree: 2020, Tulane University

URL: https://digitallibrary.tulane.edu/islandora/object/tulane:120547

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[email protected]

Ethanol consumption is known to increase the prevalence and severity of respiratory infection and impaired immunity. The relationships between ethanol exposure, vitamin D levels,… (more)

Subjects/Keywords: Systemic inflammation

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APA (6^th Edition):

Sriyotha, P. (2020). Ethanol-mediated dysregulation of cytokines and human anti-microbial peptide cathelicidin. (Thesis). Tulane University. Retrieved from https://digitallibrary.tulane.edu/islandora/object/tulane:120547

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):

Sriyotha, Phanuwat. “Ethanol-mediated dysregulation of cytokines and human anti-microbial peptide cathelicidin.” 2020. Thesis, Tulane University. Accessed April 13, 2021. https://digitallibrary.tulane.edu/islandora/object/tulane:120547.

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

MLA Handbook (7^th Edition):

Sriyotha, Phanuwat. “Ethanol-mediated dysregulation of cytokines and human anti-microbial peptide cathelicidin.” 2020. Web. 13 Apr 2021.

Vancouver:

Sriyotha P. Ethanol-mediated dysregulation of cytokines and human anti-microbial peptide cathelicidin. [Internet] [Thesis]. Tulane University; 2020. [cited 2021 Apr 13]. Available from: https://digitallibrary.tulane.edu/islandora/object/tulane:120547.

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

Council of Science Editors:

Sriyotha P. Ethanol-mediated dysregulation of cytokines and human anti-microbial peptide cathelicidin. [Thesis]. Tulane University; 2020. Available from: https://digitallibrary.tulane.edu/islandora/object/tulane:120547

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

6. Lyroni, Konstantina. Regulation of inflammation in obesity.

Degree: 2018, University of Crete (UOC); Πανεπιστήμιο Κρήτης

URL: http://hdl.handle.net/10442/hedi/43821

► Inflammation underlies a variety of physiological and pathological processes. Over the years tremendous progress has been made in understanding the cellular and molecular events that… (more)

▼ Inflammation underlies a variety of physiological and pathological processes. Over the years tremendous progress has been made in understanding the cellular and molecular events that are involved in inflammatory responses. A controlled inflammatory response is beneficial for the organism in order to maintain homeostasis, protect from infection and repair tissue damage, but it can also become detrimental if not regulated appropriately. Different instigators of inflammation, such as infection and tissue injury, are among the wide spectrum of adverse conditions that induce inflammation. In chronic inflammatory diseases such as Rheumatoid Arthritis, Systemic Lupus Erythematosus, Inflammatory Bowel Diseases and others, pathogenesis occurs due to excessive, inappropriately initiated inflammatory response. Metabolic diseases such as obesity and type II diabetes are also characterized by chronic, low-grade inflammation that has led to the concept of metabolic inflammation (metaflammation). Despite the fact that mechanisms of inflammatory response have been extensively studied, further elucidating the molecular controls of inflammation is of crucial importance. Macrophages are key players in inflammation activated by a wide spectrum of stimuli and acquire a phenotype that ranges from fully pro-inflammatory (M1) to anti-inflammatory, mediating resolution of inflammation and tissue repair (M2). Metabolic inflammation results in changes in macrophage phenotype as well. Inflammed adipose tissue has an increased number of macrophages and these macrophages are pro-inflammatory (M1-type). Effective termination of inflammation is as important as controlled initiation, therefore a plethora of factors exist that act as negative regulators. TLR signaling contributes to inflammation and metaflammation and is negatively regulated by the IL-1 Receptor Associated Kinase M (IRAK-M) protein, which acts as functional decoy to prevent phosphorylation and further signaling by IRAK-4. The world-wide epidemic of obesity has led to a dramatic increase in metabolic diseases associated with metabolic inflammation, hence deciphering the mechanisms governing processes that establish metaflammation, will allow understanding the pathogenesis of related conditions. Adipocytes are now acknowledged as more than cells for lipid storage. They have primary roles in controlling energy homeostasis and secrete hormones and lipids in order to regulate systemic metabolism. Adipose tissue is in a state of inflammation in obesity contributing to low grade systemic inflammation.Given the established importance of inflammation and metabolism in health and disease, the present study focused on analyzing the transcriptional and epigenetic mechanisms of macrophage activation focusing on the mechanisms of regulation of the intracellular TLR-signaling modulator IRAK-M (a negative regulator of the TLR4/LPS signaling). The work also aimed to decipher whether adipocytes can acquire a macrophage-like phenotype in states of inflammation such as obesity and LPS stimulation and…

Subjects/Keywords: φλεγμονή; inflammation

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APA (6^th Edition):

Lyroni, K. (2018). Regulation of inflammation in obesity. (Thesis). University of Crete (UOC); Πανεπιστήμιο Κρήτης. Retrieved from http://hdl.handle.net/10442/hedi/43821

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):

Lyroni, Konstantina. “Regulation of inflammation in obesity.” 2018. Thesis, University of Crete (UOC); Πανεπιστήμιο Κρήτης. Accessed April 13, 2021. http://hdl.handle.net/10442/hedi/43821.

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

MLA Handbook (7^th Edition):

Lyroni, Konstantina. “Regulation of inflammation in obesity.” 2018. Web. 13 Apr 2021.

Vancouver:

Lyroni K. Regulation of inflammation in obesity. [Internet] [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2018. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10442/hedi/43821.

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

Council of Science Editors:

Lyroni K. Regulation of inflammation in obesity. [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2018. Available from: http://hdl.handle.net/10442/hedi/43821

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

Texas A&M University

7. Metzger, Corinne Elizabeth. Inflammatory Bowel Disease and Bone: Mechanisms and Interventions for Inflammation-Induced Bone Alterations.

Degree: PhD, Kinesiology, 2018, Texas A&M University

URL: http://hdl.handle.net/1969.1/173354

► Inflammatory bowel disease (IBD) effects approximately 1.6 million people in the United States with the incidence and prevalence increasing worldwide. All current treatments for IBD… (more)

▼ Inflammatory bowel disease (IBD) effects approximately 1.6 million people in the United States with the incidence and prevalence increasing worldwide. All current treatments for IBD aim to simply mitigate the disease symptoms and come with negative consequences. A common comorbidity of IBD is inflammation-induced bone loss, which is characterized by increased bone resorption and decreased bone formation. Osteocytes, cells embedded in the bone matrix, are considered the primary regulatory cell type in bone; however, the role of osteocytes in inflammation-induced alterations in bone is unknown. The goals of the current project are to examine the role of osteocyte signaling proteins in inflammation-induced changes in bone turnover during chronic IBD and secondly, to explore lifestyle changes and therapeutic targets for IBD-induced alterations in bone. Male Sprague-Dawley rats (2 months old) were given gut inflammation via rectal instillations of 2,4,6-trinitrobenzenesulfonic acid (TNBS) dissolved in 30% ethanol while vehicle-treated rats received only 30% ethanol for four weeks. Osteoclast surfaces of cancellous bone were increased after TNBS while bone formation rate was decreased. These changes in bone turnover were coincident with higher osteocytes positive for pro-inflammatory markers, osteoclastogenesis regulators, and bone formation inhibitors. In a second experiment, TNBS and vehicle-treated rats were fed a moderately elevated soy protein diet during the experimental period. TNBS-treated animals fed the moderately elevated soy protein diet had reductions in osteoclast surfaces and increased bone formation rates corresponding with declines in osteocytes positive for pro-inflammatory factors. Finally, a third group of TNBS and vehicle-treated rats received exogenous administration of irisin, a protein released during exercise. TNBS-treated rats receiving irisin had significantly higher bone formation rates and lower osteoclast surfaces than those receiving TNBS alone. Additionally, irisin-treated rats had lower osteocytes positive for pro-inflammatory factors. These results indicate that osteocytes respond to inflammatory signals and may orchestrate changes in bone turnover. Secondly, a moderately elevated soy protein diet reduced the inflammatory alterations in bone during chronic IBD. Additionally, designing methods to increase endogenous irisin, possibly through exercise, could potentially reduce inflammatory changes in bone during IBD. Finally, exogenous irisin administration is a potential novel therapeutic target for inflammation-induced bone loss. Advisors/Committee Members: Bloomfield, Susan A (advisor), Fluckey, James D (committee member), Hogan, Harry A (committee member), Zawieja, David C (committee member).

Subjects/Keywords: Inflammation; Bone

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

APA (6^th Edition):

Metzger, C. E. (2018). Inflammatory Bowel Disease and Bone: Mechanisms and Interventions for Inflammation-Induced Bone Alterations. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/173354

Chicago Manual of Style (16^th Edition):

Metzger, Corinne Elizabeth. “Inflammatory Bowel Disease and Bone: Mechanisms and Interventions for Inflammation-Induced Bone Alterations.” 2018. Doctoral Dissertation, Texas A&M University. Accessed April 13, 2021. http://hdl.handle.net/1969.1/173354.

MLA Handbook (7^th Edition):

Metzger, Corinne Elizabeth. “Inflammatory Bowel Disease and Bone: Mechanisms and Interventions for Inflammation-Induced Bone Alterations.” 2018. Web. 13 Apr 2021.

Vancouver:

Metzger CE. Inflammatory Bowel Disease and Bone: Mechanisms and Interventions for Inflammation-Induced Bone Alterations. [Internet] [Doctoral dissertation]. Texas A&M University; 2018. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/1969.1/173354.

Council of Science Editors:

Metzger CE. Inflammatory Bowel Disease and Bone: Mechanisms and Interventions for Inflammation-Induced Bone Alterations. [Doctoral Dissertation]. Texas A&M University; 2018. Available from: http://hdl.handle.net/1969.1/173354

8. Schnegg, Caroline Isabel. RADIATION-INDUCED INFLAMMATORY MARKERS OF BRAIN INJURY ARE MODULATED BY PPARä ACTIVATION IN VITRO AND IN VIVO.

Degree: 2012, Wake Forest University

URL: http://hdl.handle.net/10339/37442

► As a result of improvements in cancer therapy and health care, the population of long-term cancer survivors is growing. For these approximately 12 million long-term… (more)

Subjects/Keywords: Inflammation

…and Inflammation Classically, radiation-induced late normal tissue injury was thought to be… …which contribute to increased oxidative stress and inflammation [36-38]. This model… …act as second messengers to induce inflammation [43]. Although it was once… …believed that the brain was not susceptible to inflammation, it is now recognized that… …and/or inflammation, therefore, appears to be one of the mechanisms underlying radiation…

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APA (6^th Edition):

Schnegg, C. I. (2012). RADIATION-INDUCED INFLAMMATORY MARKERS OF BRAIN INJURY ARE MODULATED BY PPARä ACTIVATION IN VITRO AND IN VIVO. (Thesis). Wake Forest University. Retrieved from http://hdl.handle.net/10339/37442

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):

Schnegg, Caroline Isabel. “RADIATION-INDUCED INFLAMMATORY MARKERS OF BRAIN INJURY ARE MODULATED BY PPARä ACTIVATION IN VITRO AND IN VIVO.” 2012. Thesis, Wake Forest University. Accessed April 13, 2021. http://hdl.handle.net/10339/37442.

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

MLA Handbook (7^th Edition):

Schnegg, Caroline Isabel. “RADIATION-INDUCED INFLAMMATORY MARKERS OF BRAIN INJURY ARE MODULATED BY PPARä ACTIVATION IN VITRO AND IN VIVO.” 2012. Web. 13 Apr 2021.

Vancouver:

Schnegg CI. RADIATION-INDUCED INFLAMMATORY MARKERS OF BRAIN INJURY ARE MODULATED BY PPARä ACTIVATION IN VITRO AND IN VIVO. [Internet] [Thesis]. Wake Forest University; 2012. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10339/37442.

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

Council of Science Editors:

Schnegg CI. RADIATION-INDUCED INFLAMMATORY MARKERS OF BRAIN INJURY ARE MODULATED BY PPARä ACTIVATION IN VITRO AND IN VIVO. [Thesis]. Wake Forest University; 2012. Available from: http://hdl.handle.net/10339/37442

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

9. Gauthier, Alexandre. Rôle des protéases à sérine du polynucléaire neutrophile dans l'inflammation associée à la mucoviscidose : No title available.

Degree: Docteur es, Sciences de la vie et de la santé, spécialité Biochimie, 2009, Université François-Rabelais de Tours

URL: http://www.theses.fr/2009TOUR4040

►

La mucoviscidose est une maladie génétique caractérisée par une inflammation pulmonairepersistante du poumon résultant d’un recrutement massif de polynucléaires neutrophiles quisécrètent trois protéases à sérine,… (more)

Subjects/Keywords: NETs; Inflammation

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APA (6^th Edition):

Gauthier, A. (2009). Rôle des protéases à sérine du polynucléaire neutrophile dans l'inflammation associée à la mucoviscidose : No title available. (Doctoral Dissertation). Université François-Rabelais de Tours. Retrieved from http://www.theses.fr/2009TOUR4040

Chicago Manual of Style (16^th Edition):

Gauthier, Alexandre. “Rôle des protéases à sérine du polynucléaire neutrophile dans l'inflammation associée à la mucoviscidose : No title available.” 2009. Doctoral Dissertation, Université François-Rabelais de Tours. Accessed April 13, 2021. http://www.theses.fr/2009TOUR4040.

MLA Handbook (7^th Edition):

Gauthier, Alexandre. “Rôle des protéases à sérine du polynucléaire neutrophile dans l'inflammation associée à la mucoviscidose : No title available.” 2009. Web. 13 Apr 2021.

Vancouver:

Gauthier A. Rôle des protéases à sérine du polynucléaire neutrophile dans l'inflammation associée à la mucoviscidose : No title available. [Internet] [Doctoral dissertation]. Université François-Rabelais de Tours; 2009. [cited 2021 Apr 13]. Available from: http://www.theses.fr/2009TOUR4040.

Council of Science Editors:

Gauthier A. Rôle des protéases à sérine du polynucléaire neutrophile dans l'inflammation associée à la mucoviscidose : No title available. [Doctoral Dissertation]. Université François-Rabelais de Tours; 2009. Available from: http://www.theses.fr/2009TOUR4040

10. Molnarfi, Nicolas. Production of pro- and anti-inflammatory cytokines in human monocytes: regulation and signaling.

Degree: 2005, Université de Genève

URL: http://doc.rero.ch/record/5559

► Les tissus vivants répondent aux agressions par l'inflammation qui élimine les agents préjudiciables et initie la guérison des tissus lésés. Les dérèglements de l'inflammation entraînent… (more)

Subjects/Keywords: inflammation

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APA (6^th Edition):

Molnarfi, N. (2005). Production of pro- and anti-inflammatory cytokines in human monocytes: regulation and signaling. (Thesis). Université de Genève. Retrieved from http://doc.rero.ch/record/5559

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):

Molnarfi, Nicolas. “Production of pro- and anti-inflammatory cytokines in human monocytes: regulation and signaling.” 2005. Thesis, Université de Genève. Accessed April 13, 2021. http://doc.rero.ch/record/5559.

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

MLA Handbook (7^th Edition):

Molnarfi, Nicolas. “Production of pro- and anti-inflammatory cytokines in human monocytes: regulation and signaling.” 2005. Web. 13 Apr 2021.

Vancouver:

Molnarfi N. Production of pro- and anti-inflammatory cytokines in human monocytes: regulation and signaling. [Internet] [Thesis]. Université de Genève; 2005. [cited 2021 Apr 13]. Available from: http://doc.rero.ch/record/5559.

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

Council of Science Editors:

Molnarfi N. Production of pro- and anti-inflammatory cytokines in human monocytes: regulation and signaling. [Thesis]. Université de Genève; 2005. Available from: http://doc.rero.ch/record/5559

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

University of Houston

11. Zambrano Cobo, Amarayca. Inflammation in Zebrafish Models.

Degree: MS, Biomedical Engineering, 2015, University of Houston

URL: http://hdl.handle.net/10657/4848

► The zebrafish is an outstanding model for in-vivo imaging of inflammation due to its optical translucency and the ability of transgenic lines to express fluorescent… (more)

Subjects/Keywords: Zebrafish; Inflammation

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

APA (6^th Edition):

Zambrano Cobo, A. (2015). Inflammation in Zebrafish Models. (Masters Thesis). University of Houston. Retrieved from http://hdl.handle.net/10657/4848

Chicago Manual of Style (16^th Edition):

Zambrano Cobo, Amarayca. “Inflammation in Zebrafish Models.” 2015. Masters Thesis, University of Houston. Accessed April 13, 2021. http://hdl.handle.net/10657/4848.

MLA Handbook (7^th Edition):

Zambrano Cobo, Amarayca. “Inflammation in Zebrafish Models.” 2015. Web. 13 Apr 2021.

Vancouver:

Zambrano Cobo A. Inflammation in Zebrafish Models. [Internet] [Masters thesis]. University of Houston; 2015. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10657/4848.

Council of Science Editors:

Zambrano Cobo A. Inflammation in Zebrafish Models. [Masters Thesis]. University of Houston; 2015. Available from: http://hdl.handle.net/10657/4848

University of Manitoba

12. Balhara, Jyoti. Role of PTX3 in allergic airway inflammation.

Degree: Immunology, 2013, University of Manitoba

URL: http://hdl.handle.net/1993/31935

► Thesis Abstract: Pentraxin 3 (PTX3) is a pattern recognition receptor that plays an important role in providing immunity against various pulmonary inflammatory conditions. Having known… (more)

▼ Thesis Abstract: Pentraxin 3 (PTX3) is a pattern recognition receptor that plays an important role in providing immunity against various pulmonary inflammatory conditions. Having known its role in fostering lung immunity, aim of my PhD thesis was to examine the role of PTX3 in asthma. In my thesis, I showed an enhanced level of PTX3 in the airway fluid of severe asthmatics and also in the airway fluid and the lungs of allergen exposed mice. To further investigate the role of PTX3, I used a murine model of ovalbumin (OVA)-induced experimental asthma and performed experiments on PTX3+/+ and PTX3-/- mice. I observed an enhanced airway inflammation and hyperactivity in OVA-exposed PTX3 Knockout (PTX3-/-) mice. In PTX3-/- mice, there was an IL-17A dominant inflammation as compared to PTX3+/+ mice upon OVA challenge. This response was accompanied with increased CD4 T cell survival and reduced IL-2 production by these cells. As Th17 phenotype of CD4 T cells is shaped by IL-6 and IL-23 producing dendritic cells, we observed increased preponderance of such DCs in the lungs and the draining lymph nodes of PTX3-/- mice as compared to their PTX3+/+ counterparts, plausibly supporting Th17/ IL-17A dominant inflammation in the former. Furthermore, there was increased infiltration of inflammatory DCs in the lungs in PTX3-/- mice upon OVA exposure. This observation was in line with increased generation of common myeloid progenitors in the bone marrow of these mice. PTX3-/- DCs showed reduced MHCII expression but increased surface expression of CD80 and CD86 along with increased ability of PTX3-/- DCs to uptake and process OVA. Since these DCs showed increase IL-6 and IL-23 production, co-culture of PTX3-/- DCs with OT II CD4 T cells resulted in greater IL-17A production as compared to those that were co-cultured with PTX3+/+ DCs. Altogether, I have observed that deletion of PTX3 resulted in enhanced IL-17 immune response plausibly through increased IL-6 and IL-23 producing DCs in OVA-exposed mice. In summary, findings of my thesis provide insights of the novel regulatory role of PTX3 in allergic inflammation, primarily in context with CD4 T cell-DC axis. Advisors/Committee Members: Soussi Gounni, Abdelilah (Immunology) (supervisor), Uzonna, Jude (Immunology) Mookherjee, Neeloffer (Immunology).

Subjects/Keywords: asthma; inflammation

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

APA (6^th Edition):

Balhara, J. (2013). Role of PTX3 in allergic airway inflammation. (Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/31935

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):

Balhara, Jyoti. “Role of PTX3 in allergic airway inflammation.” 2013. Thesis, University of Manitoba. Accessed April 13, 2021. http://hdl.handle.net/1993/31935.

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

MLA Handbook (7^th Edition):

Balhara, Jyoti. “Role of PTX3 in allergic airway inflammation.” 2013. Web. 13 Apr 2021.

Vancouver:

Balhara J. Role of PTX3 in allergic airway inflammation. [Internet] [Thesis]. University of Manitoba; 2013. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/1993/31935.

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

Council of Science Editors:

Balhara J. Role of PTX3 in allergic airway inflammation. [Thesis]. University of Manitoba; 2013. Available from: http://hdl.handle.net/1993/31935

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

University of Saskatchewan

13. Bailey, Georgia C. Assessment of Heat Shock Proteins in Human Myometrial Cells under Pro-Inflammatory Conditions and their Presence in Extracellular Vesicles.

Degree: 2020, University of Saskatchewan

URL: http://hdl.handle.net/10388/13165

► During pregnancy the myometrium undergoes a program of differentiation in parallel with immune system transformation. The end result is the production of a powerfully contractile… (more)

▼ During pregnancy the myometrium undergoes a program of differentiation in parallel with immune system transformation. The end result is the production of a powerfully contractile tissue able to deliver a term fetus. Small heat shock proteins (sHSPs) are a family of 10 proteins (HSPB1-10) involved in regulating stress responses in tissues, including inflammation, and may take part in intercellular communication via extracellular vesicles (EVs). Since HSPB1 and HSPB5 are highly expressed in myometrium during late pregnancy and labour, it was hypothesized that HSPB1 and HSPB5 expression would be induced in myometrial cells by a pro- inflammatory stimulus, in correlation with the Nuclear Factor kappa B (NF-kB) signaling pathway. Based on the literature, it was also hypothesized that these proteins would be released extracellularly in EVs. Immortalized human myometrial cells (hTERT-HM) were incubated with 1 ng/ml of IL-1β or vehicle for 0.5, 1, 3, or 6 hours (h). The expression of sHSPs and markers of inflammation in these cells were then assessed by immunoblot analysis. Detection of pSer82- HSPB1 and pSer59-HSPB5 proteins was significantly elevated in cells at 0.5 h of cytokine incubation compared to vehicle control. Activation of NF-kB, marked by phosphorylation on serine-536, was also significantly elevated after 0.5 h. In contrast, inhibitor of kappa B (IkB) expression was significantly decreased after 1 h of cytokine incubation. Thus, pSer82-HSPB1 and pSer59-HSPB5 levels correlate with NF-kB activation. Analysis of cell conditioned culture media in this experimental model also demonstrated myometrial cell secretion of EVs. Scanning electron microscopy and transmission electron microscopy verified EVs as round vesicles of 20 to 200 nm in diameter regardless of whether or not cells were exposed to IL-1β. Immunoblot analysis demonstrated EVs contained the markers cluster of differentiation 63 (CD63), apoptosis linked gene 2-interacting protein X (ALIX), and tumor susceptibility gene 101 (TSG101). ii Furthermore, HSP90, HSP70, HSPB1, and NF-kB were all detected in EVs as cargo for extracellular release. These results suggest a novel mechanism of myometrial cell intercellular communication during pregnancy that could help modulate the pro-inflammatory response in the myometrium at labour. Advisors/Committee Members: MacPhee, Daniel, Slater, Donna, Unniappan, Suraj, Wilson, Heather.

Subjects/Keywords: Myometrium; Inflammation

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APA (6^th Edition):

Bailey, G. C. (2020). Assessment of Heat Shock Proteins in Human Myometrial Cells under Pro-Inflammatory Conditions and their Presence in Extracellular Vesicles. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/13165

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):

Bailey, Georgia C. “Assessment of Heat Shock Proteins in Human Myometrial Cells under Pro-Inflammatory Conditions and their Presence in Extracellular Vesicles.” 2020. Thesis, University of Saskatchewan. Accessed April 13, 2021. http://hdl.handle.net/10388/13165.

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

MLA Handbook (7^th Edition):

Bailey, Georgia C. “Assessment of Heat Shock Proteins in Human Myometrial Cells under Pro-Inflammatory Conditions and their Presence in Extracellular Vesicles.” 2020. Web. 13 Apr 2021.

Vancouver:

Bailey GC. Assessment of Heat Shock Proteins in Human Myometrial Cells under Pro-Inflammatory Conditions and their Presence in Extracellular Vesicles. [Internet] [Thesis]. University of Saskatchewan; 2020. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10388/13165.

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

Council of Science Editors:

Bailey GC. Assessment of Heat Shock Proteins in Human Myometrial Cells under Pro-Inflammatory Conditions and their Presence in Extracellular Vesicles. [Thesis]. University of Saskatchewan; 2020. Available from: http://hdl.handle.net/10388/13165

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

Rutgers University

14. Boyanapalli, Sarandeep S S. Anti-inflammatory, epigenetic regulatory role of phytochemicals and pkpd modeling of pharmacological effects.

Degree: PhD, Pharmaceutical Science, 2016, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/49917/

►

Chronic inflammation is considered to play an important factor in neoplastic progression via the induction of reactive oxygen, reactive nitrogen species and induction of growth… (more)

▼

Chronic inflammation is considered to play an important factor in neoplastic progression via the induction of reactive oxygen, reactive nitrogen species and induction of growth promoting cytokines. Thus, it is very important to develop new drugs that can inhibit inflammation and prevent cancer formation or progression. Dietary phytochemicals are derived from natural sources and are found commonly in the fruits and vegetables consumed regularly as part of the diet. Understanding the mechanism by which the natural compounds inhibit inflammation and prevent cancers is very important and could pave way to developing new targets and drugs for chemoprevention. During my dissertation, I have studied the anti-inflammatory properties of phytochemicals like Curcumin, Phenethylisothiocyanate (PEITC) and Ursolic acid (UA). The importance of Nrf2, a transcription factor in attenuating inflammation was studied using macrophages from Nrf2 (+/+) and Nrf2 (-/-) mice. The results showed that Nrf2 plays a major role in the anti-inflammatory effects of Curcumin and PEITC as seen from the differences between Nrf2 (+/+) and Nrf2 (-/-) mice macrophages. The anti-inflammatory effect of Curcumin was further evaluated iii in rats. The results showed that Curcumin suppressed lipopolysaccharide (LPS) induced inflammation as well as some epigenetic modifying genes like DNA methyltransferases and Histone deacetylases. The pharmacological response was modeled using an indirect response approach.The epigenetic modulatory role of PEITC was tested in LNCaP (androgne sensitive human prostate adenocarcinoma) cells, the results revealed that PEITC inhibits DNA methylation and increased transcription of RASSF1A, a tumor suppressor gene and in turn promotes apoptosis. Ursolic acid (UA), a pentacyclic triterpenoid was studied for its anti-inflammatory and epigeneitc modulatory role in PTEN-CaP2 cells (Prostate specific PTEN null epithelial cell line). UA suppressed LPS induced inflammatory cytokines as well as inhibited HDAC protein expression along with increasing the expression of Nrf2 a master regulator of anti-oxidate stress response pathway and NQO1. Collectively, the results demonstrated the anti-inflammatory and epigenetic modulatory potential of phytochemicals in vitro and in vivo.

Advisors/Committee Members: Kong, Ah-Ng Tony (chair), Hatefi, Arasha (internal member), Androulakis, Ioannis P (internal member), Verzi, Michael (outside member).

Subjects/Keywords: Phytochemicals; Inflammation

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

APA (6^th Edition):

Boyanapalli, S. S. S. (2016). Anti-inflammatory, epigenetic regulatory role of phytochemicals and pkpd modeling of pharmacological effects. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/49917/

Chicago Manual of Style (16^th Edition):

Boyanapalli, Sarandeep S S. “Anti-inflammatory, epigenetic regulatory role of phytochemicals and pkpd modeling of pharmacological effects.” 2016. Doctoral Dissertation, Rutgers University. Accessed April 13, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/49917/.

MLA Handbook (7^th Edition):

Boyanapalli, Sarandeep S S. “Anti-inflammatory, epigenetic regulatory role of phytochemicals and pkpd modeling of pharmacological effects.” 2016. Web. 13 Apr 2021.

Vancouver:

Boyanapalli SSS. Anti-inflammatory, epigenetic regulatory role of phytochemicals and pkpd modeling of pharmacological effects. [Internet] [Doctoral dissertation]. Rutgers University; 2016. [cited 2021 Apr 13]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/49917/.

Council of Science Editors:

Boyanapalli SSS. Anti-inflammatory, epigenetic regulatory role of phytochemicals and pkpd modeling of pharmacological effects. [Doctoral Dissertation]. Rutgers University; 2016. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/49917/

15. Benkdane, Merieme. Rôle protecteur des cellules de Küpffer de phénotype M2 anti-inflammatoire dans la maladie alcoolique du foie : Protective role of M2 anti-inflammatory Kupffer cells in alcoholic liver disease.

Degree: Docteur es, Physiopathologie, 2012, Université Paris-Est

URL: http://www.theses.fr/2012PEST0062

► L'alcool est la première cause de maladie hépatique en France, et la maladie alcoolique du foie est responsable de près de 7000 décès par an.… (more)

▼ L'alcool est la première cause de maladie hépatique en France, et la maladie alcoolique du foie est responsable de près de 7000 décès par an. La surcharge graisseuse est la troisième cause de maladie hépatique, et s'inscrit dans le cadre plus large du syndrome métabolique. La physiopathologie de ces deux types de maladies hépatiques est très similaire. La stéatose, définie par l'accumulation excessive de triglycérides dans le foie, est la première lésion retrouvée chez les patients. La stéatose peut évoluer vers la stéato‐hépatite lorsqu'elle est associée à une inflammation, une mort hépatocytaire, et à l'initiation d'une réponse fibrogénique. La stéato‐hépatite évolue parfois vers la cirrhose, stade ultime avant le carcinome hépatocellulaire. Il n'existe à ce jour aucun traitement efficace de ces maladies hormis le sevrage alcoolique dans le cadre de la maladie alcoolique du foie et un régime associé à de l'exercice dans le cadre de la maladie hépatique d'origine non‐alcoolique. Il est donc urgent d'identifier de nouvelles stratégies thérapeutiques pour lutter contre la progression de ces maladies.L'activation des cellules de Küpffer, les macrophages résidents du foie, joue un rôle déterminant dans le processus inflammatoire qui initie l'atteinte hépatique. Comme tous les macrophages, les cellules de Küpffer peuvent adopter tout un spectre de phénotypes parmi lesquels on distingue deux extrêmes : le phénotype M1 ou pro‐inflammatoire et le phénotype M2 ou anti‐inflammatoire. Les données de la littérature ainsi que celles préalablement obtenues par le laboratoire d'accueil ont établi les effets délétères d'une polarisation pro‐inflammatoire M1 des cellules de Küpffer sur l'évolution de la maladie hépatique d'origine alcoolique ou non alcoolique. Cependant, aucune étude n'avait examiné l'impact d'une polarisation anti‐inflammatoire (M2) des cellules de Küpffer sur ces maladies.L'objectif de ce travail a été d'évaluer si favoriser la polarisation des cellules de Küpffer vers un phénotype M2 anti‐inflammatoire pouvait limiter la progression des maladies hépatiques d'origine alcoolique ou non alcoolique.Afin de mener à bien ce projet, nous avons combiné l'utilisation de modèles murins de maladie hépatique d'origine alcoolique ou non alcoolique, des approches pharmacologiques et des expériences sur cellules isolées. Ces études ont été complétées par des données obtenues sur des biopsies humaines.Ce travail a permis de démontrer que favoriser la polarisation M2 des cellules de Küpffer protège le foie de la stéatose, de la mort hépatocytaire et de l'inflammation. Ces résultats identifient un nouveau mécanisme anti‐inflammatoire déclenché par les cellules de Küpffer polarisées M2 : l'induction sélective de l'apoptose des cellules de Küpffer polarisées M1. Ce travail ouvre de nouvelles perspectives à l'identification de stratégies pour limiter la progression des maladies hépatiques et pourrait également avoir des retombées plus larges dans le cadre d'autres maladies chroniques inflammatoires ciblant d'autres tissus que le… Advisors/Committee Members: Pavoine, Catherine (thesis director).

Subjects/Keywords: Alcool; Macrophages; Inflammation; Alcohol; Macrophages; Inflammation; 616.3

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

APA (6^th Edition):

Benkdane, M. (2012). Rôle protecteur des cellules de Küpffer de phénotype M2 anti-inflammatoire dans la maladie alcoolique du foie : Protective role of M2 anti-inflammatory Kupffer cells in alcoholic liver disease. (Doctoral Dissertation). Université Paris-Est. Retrieved from http://www.theses.fr/2012PEST0062

Chicago Manual of Style (16^th Edition):

Benkdane, Merieme. “Rôle protecteur des cellules de Küpffer de phénotype M2 anti-inflammatoire dans la maladie alcoolique du foie : Protective role of M2 anti-inflammatory Kupffer cells in alcoholic liver disease.” 2012. Doctoral Dissertation, Université Paris-Est. Accessed April 13, 2021. http://www.theses.fr/2012PEST0062.

MLA Handbook (7^th Edition):

Benkdane, Merieme. “Rôle protecteur des cellules de Küpffer de phénotype M2 anti-inflammatoire dans la maladie alcoolique du foie : Protective role of M2 anti-inflammatory Kupffer cells in alcoholic liver disease.” 2012. Web. 13 Apr 2021.

Vancouver:

Benkdane M. Rôle protecteur des cellules de Küpffer de phénotype M2 anti-inflammatoire dans la maladie alcoolique du foie : Protective role of M2 anti-inflammatory Kupffer cells in alcoholic liver disease. [Internet] [Doctoral dissertation]. Université Paris-Est; 2012. [cited 2021 Apr 13]. Available from: http://www.theses.fr/2012PEST0062.

Council of Science Editors:

Benkdane M. Rôle protecteur des cellules de Küpffer de phénotype M2 anti-inflammatoire dans la maladie alcoolique du foie : Protective role of M2 anti-inflammatory Kupffer cells in alcoholic liver disease. [Doctoral Dissertation]. Université Paris-Est; 2012. Available from: http://www.theses.fr/2012PEST0062

University of Guelph

16. Hann, Melissa. Anti-inflammatory Activity of Isomaltodextrin in a C57BL/6NCrl Mouse Model with Lipopolysaccharide-induced Low-grade Chronic Inflammation.

Degree: MS, Department of Food Science, 2018, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/14124

► The purpose of this study was to identify the anti-inflammatory activity and mechanism of isomaltodextrin in a C57BL/6NCrl mouse model with lipopolysaccharide-induced systemic low-grade chronic… (more)

Subjects/Keywords: isomaltodextrin; low-grade inflammation; chronic inflammation; prebiotic

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

APA (6^th Edition):

Hann, M. (2018). Anti-inflammatory Activity of Isomaltodextrin in a C57BL/6NCrl Mouse Model with Lipopolysaccharide-induced Low-grade Chronic Inflammation. (Masters Thesis). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/14124

Chicago Manual of Style (16^th Edition):

Hann, Melissa. “Anti-inflammatory Activity of Isomaltodextrin in a C57BL/6NCrl Mouse Model with Lipopolysaccharide-induced Low-grade Chronic Inflammation.” 2018. Masters Thesis, University of Guelph. Accessed April 13, 2021. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/14124.

MLA Handbook (7^th Edition):

Hann, Melissa. “Anti-inflammatory Activity of Isomaltodextrin in a C57BL/6NCrl Mouse Model with Lipopolysaccharide-induced Low-grade Chronic Inflammation.” 2018. Web. 13 Apr 2021.

Vancouver:

Hann M. Anti-inflammatory Activity of Isomaltodextrin in a C57BL/6NCrl Mouse Model with Lipopolysaccharide-induced Low-grade Chronic Inflammation. [Internet] [Masters thesis]. University of Guelph; 2018. [cited 2021 Apr 13]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/14124.

Council of Science Editors:

Hann M. Anti-inflammatory Activity of Isomaltodextrin in a C57BL/6NCrl Mouse Model with Lipopolysaccharide-induced Low-grade Chronic Inflammation. [Masters Thesis]. University of Guelph; 2018. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/14124

University of California – Merced

17. Al-Kuhlani, Mufadhal Mohammed. Negative Regulators of Toll-Like Receptors During Chlamydia trachomatis Infection.

Degree: Quantitative and Systems Biology, 2013, University of California – Merced

URL: http://www.escholarship.org/uc/item/1m5036rd

► Chlamydia trachomatis is the most common bacterial sexually-transmitted disease (STD) around the world. The response of the immune system to eliminate C. trachomatis infection through… (more)

▼ Chlamydia trachomatis is the most common bacterial sexually-transmitted disease (STD) around the world. The response of the immune system to eliminate C. trachomatis infection through inflammation is a very efficient process. However, persistent infection or uncontrolled inflammation causes a complication in the upper genital tract, which can ultimately lead to infertility and chronic pelvic pain. Therefore, inflammation has to be tightly regulated to avoid an uncontrolled immune response. The genetic factors that regulate inflammation during Chlamydia infection have not been clearly characterized. SIGIRR, Triad3A and TRAIL-R are proteins that have been shown to manipulate inflammation in response to various pathogens and diseases. However, little is known about their role during C. trachomatis infection.Our results indicate that in the absence of SIGIRR, epithelial cells induce higher levels of proinflammatory cytokines in response to chlamydia infection. In addition, overexpression analysis reveals that SIGIRR associates with MyD88 and localizes around the inclusion of the Chlamydia and the nucleus of the infected cell. Additionally, our data indicates that the absence of Triad3A in HEK cells that express individual TLRs does not affect the levels of IL-8 in TLR2, TLR3 or TLR4, when activated by C. trachomatis. However, the absence of Triad3A in cells that express both TLR2 and TLR4 induces lower level of IL-8 compared to wild type cells as a result of the inhibitory effect that TLR4 exerts on TLR2.Ex-vivo analysis shows that Chlamydia infection of bone marrow derived macrophages (BMDM) and primary lung fibroblasts from TRAIL-R deficient mice, induces higher levels of MIP2 mRNA expression and IL-1β secretion compared to cells from the wild type mice. In addition, in vitro study of human TRAILR1 shows that reduction of TRAIL-R1 expression on HeLa cells correlates with an increase of IL-8 expression and secretion in Chlamydia-infected cells.Taken together, our data shows that SIGIRR, Triad3A and for the first time human TRAIL-R1, function as regulators of the immune response to C. trachomatis infection. This finding provides an insight into the immune-pathogenesis ofC. trachomatis that can be used to develop novel intervention and diagnostic strategies to treat and identify individuals at high risk.

Subjects/Keywords: Immunology; Chlamydia; Inflammation

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APA (6^th Edition):

Al-Kuhlani, M. M. (2013). Negative Regulators of Toll-Like Receptors During Chlamydia trachomatis Infection. (Thesis). University of California – Merced. Retrieved from http://www.escholarship.org/uc/item/1m5036rd

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):

Al-Kuhlani, Mufadhal Mohammed. “Negative Regulators of Toll-Like Receptors During Chlamydia trachomatis Infection.” 2013. Thesis, University of California – Merced. Accessed April 13, 2021. http://www.escholarship.org/uc/item/1m5036rd.

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

MLA Handbook (7^th Edition):

Al-Kuhlani, Mufadhal Mohammed. “Negative Regulators of Toll-Like Receptors During Chlamydia trachomatis Infection.” 2013. Web. 13 Apr 2021.

Vancouver:

Al-Kuhlani MM. Negative Regulators of Toll-Like Receptors During Chlamydia trachomatis Infection. [Internet] [Thesis]. University of California – Merced; 2013. [cited 2021 Apr 13]. Available from: http://www.escholarship.org/uc/item/1m5036rd.

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

Council of Science Editors:

Al-Kuhlani MM. Negative Regulators of Toll-Like Receptors During Chlamydia trachomatis Infection. [Thesis]. University of California – Merced; 2013. Available from: http://www.escholarship.org/uc/item/1m5036rd

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

University of Utah

18. Osborne, Amber Valeria. The Modulatory Role of Neuronal Nicotinic Receptors on Peripheral Inflammation.

Degree: PhD, Pathology;, 2010, University of Utah

URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/1089/rec/1195

► This dissertation examines the relationship between inflammatory cytokines and nicotinic acetylcholine receptors (nAChR). WT and nAChRa7 null mice were exposed to 4.8kJ/m2 of UVB on… (more)

▼ This dissertation examines the relationship between inflammatory cytokines and nicotinic acetylcholine receptors (nAChR). WT and nAChRa7 null mice were exposed to 4.8kJ/m2 of UVB on a standardized area of back skin. This dose of UVB caused the skin to be visibly inflamed 48 hours after exposure; at this point the back skin was removed and analyzed for inflammatory cytokines. Production of IL-lp and IL-6, but not TNFa was significantly increased in a 7 null mice. Further, H&E stained skin sections revealed greater edema in mice lacking a7. Production of SOCS3, a negative regulator of cytokines, was decreased in inflamed skin from a7 null mice, suggesting a potential mechanism by which a7 could regulate cytokine production. The induction of IL-1(3 and IL-6 in skin by UVB was inhibited in mice first exposed to y-irradiation, suggesting that rapidly dividing cells that infiltrate the inflamed skin were responsible for the measured cytokine production. To further identify the types of cells infiltrating the skin following an inflammatory stimulus, croton oil was applied to mouse ears and infiltrating cells were isolated following the separation of dorsal and ventral ear flaps. Mice lacking a7 had a significant increase in the total number of recruited cells as well as increased expression of IL-lp, IL-6 and TNFa by infiltrating cells. The cells infiltrating the inflamed site were determined to be CD1 lb+ Ly6g+ neutrophils and CD1 lb+ F4/80+ macrophages by FACS analysis. Further, it was determined that chemokines which recruit neutrophils and macrophages, such as CXCL2, CXCL5 and CCL3 were all also increased in a7 null mice. Inhibiting the p38 MAP Kinase signaling pathway in WT and a 7 null primary macrophage cultures decreased the LPS induced expression of cytokines and chemokines. The reciprocal effect of cytokines on nicotinic receptors was also investigated. It was determined that treatment of transfected HEK293 cells with TNFa induces enhanced upregulation of the high affinity nicotine binding receptor a4p2. Treatment of these cells with a p38 MAP Kinase inhibitor blocks the TNFa enhanced upregulation. Collectively, these data demonstrate a relationship between nicotinic receptors and inflammatory cytokines and the involvement of the p38 MAP Kinase pathway.

Subjects/Keywords: Nicotine Receptors; Inflammation

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APA (6^th Edition):

Osborne, A. V. (2010). The Modulatory Role of Neuronal Nicotinic Receptors on Peripheral Inflammation. (Doctoral Dissertation). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/1089/rec/1195

Chicago Manual of Style (16^th Edition):

Osborne, Amber Valeria. “The Modulatory Role of Neuronal Nicotinic Receptors on Peripheral Inflammation.” 2010. Doctoral Dissertation, University of Utah. Accessed April 13, 2021. http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/1089/rec/1195.

MLA Handbook (7^th Edition):

Osborne, Amber Valeria. “The Modulatory Role of Neuronal Nicotinic Receptors on Peripheral Inflammation.” 2010. Web. 13 Apr 2021.

Vancouver:

Osborne AV. The Modulatory Role of Neuronal Nicotinic Receptors on Peripheral Inflammation. [Internet] [Doctoral dissertation]. University of Utah; 2010. [cited 2021 Apr 13]. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/1089/rec/1195.

Council of Science Editors:

Osborne AV. The Modulatory Role of Neuronal Nicotinic Receptors on Peripheral Inflammation. [Doctoral Dissertation]. University of Utah; 2010. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/1089/rec/1195

University of Alberta

19. van Diepen, Sean. The prognosis and outcomes of patients with a ST-segment elevation myocardial infarction and the biochemical and clinical inflammatory response.

Degree: MS, Department of Medicine, 2013, University of Alberta

URL: https://era.library.ualberta.ca/files/h702q735f

► Acute myocardial infarction, and specifically coronary plaque rupture, has been associated with a systemic inflammatory cascade. Using multiple large clinical trial datasets, we sought to… (more)

Subjects/Keywords: myocardial infarction; inflammation

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APA (6^th Edition):

van Diepen, S. (2013). The prognosis and outcomes of patients with a ST-segment elevation myocardial infarction and the biochemical and clinical inflammatory response. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/h702q735f

Chicago Manual of Style (16^th Edition):

van Diepen, Sean. “The prognosis and outcomes of patients with a ST-segment elevation myocardial infarction and the biochemical and clinical inflammatory response.” 2013. Masters Thesis, University of Alberta. Accessed April 13, 2021. https://era.library.ualberta.ca/files/h702q735f.

MLA Handbook (7^th Edition):

van Diepen, Sean. “The prognosis and outcomes of patients with a ST-segment elevation myocardial infarction and the biochemical and clinical inflammatory response.” 2013. Web. 13 Apr 2021.

Vancouver:

van Diepen S. The prognosis and outcomes of patients with a ST-segment elevation myocardial infarction and the biochemical and clinical inflammatory response. [Internet] [Masters thesis]. University of Alberta; 2013. [cited 2021 Apr 13]. Available from: https://era.library.ualberta.ca/files/h702q735f.

Council of Science Editors:

van Diepen S. The prognosis and outcomes of patients with a ST-segment elevation myocardial infarction and the biochemical and clinical inflammatory response. [Masters Thesis]. University of Alberta; 2013. Available from: https://era.library.ualberta.ca/files/h702q735f

Universiteit Utrecht

20. Emans, T.W. Inflammation in salt-induced hypertension.

Degree: 2014, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/289594

► Hypertension in the human population became like a worldwide epidemic, increasing risk for cardiovascular diseases. The most important contributor to hypertension among life style factors… (more)

Subjects/Keywords: salt; hypertension; inflammation

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APA (6^th Edition):

Emans, T. W. (2014). Inflammation in salt-induced hypertension. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/289594

Chicago Manual of Style (16^th Edition):

Emans, T W. “Inflammation in salt-induced hypertension.” 2014. Masters Thesis, Universiteit Utrecht. Accessed April 13, 2021. http://dspace.library.uu.nl:8080/handle/1874/289594.

MLA Handbook (7^th Edition):

Emans, T W. “Inflammation in salt-induced hypertension.” 2014. Web. 13 Apr 2021.

Vancouver:

Emans TW. Inflammation in salt-induced hypertension. [Internet] [Masters thesis]. Universiteit Utrecht; 2014. [cited 2021 Apr 13]. Available from: http://dspace.library.uu.nl:8080/handle/1874/289594.

Council of Science Editors:

Emans TW. Inflammation in salt-induced hypertension. [Masters Thesis]. Universiteit Utrecht; 2014. Available from: http://dspace.library.uu.nl:8080/handle/1874/289594

Cornell University

21. Sinha, Siddhartha. Role Of Substrate Stiffness In Driving Atherogenic Behavior In Macrophages.

Degree: M.S., Physiology, Physiology, 2014, Cornell University

URL: http://hdl.handle.net/1813/37128

► Atherosclerosis is a decades-long process whose patients often remain asymptomatic until after a heart attack or stroke. Novel therapeutic approaches focus on tuning the body's… (more)

Subjects/Keywords: Atherosclerosis; Inflammation; Macrophage

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APA (6^th Edition):

Sinha, S. (2014). Role Of Substrate Stiffness In Driving Atherogenic Behavior In Macrophages. (Masters Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/37128

Chicago Manual of Style (16^th Edition):

Sinha, Siddhartha. “Role Of Substrate Stiffness In Driving Atherogenic Behavior In Macrophages.” 2014. Masters Thesis, Cornell University. Accessed April 13, 2021. http://hdl.handle.net/1813/37128.

MLA Handbook (7^th Edition):

Sinha, Siddhartha. “Role Of Substrate Stiffness In Driving Atherogenic Behavior In Macrophages.” 2014. Web. 13 Apr 2021.

Vancouver:

Sinha S. Role Of Substrate Stiffness In Driving Atherogenic Behavior In Macrophages. [Internet] [Masters thesis]. Cornell University; 2014. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/1813/37128.

Council of Science Editors:

Sinha S. Role Of Substrate Stiffness In Driving Atherogenic Behavior In Macrophages. [Masters Thesis]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/37128

Cornell University

22. Mitchell, Michael. Mechanotransduction And Therapeutic Targeting Of Cells In The Circulation.

Degree: PhD, Biomedical Engineering, 2014, Cornell University

URL: http://hdl.handle.net/1813/39384

► The application of fluid shear stress on leukocytes and tumor cells in the circulation plays a critical role in the progression of inflammation and cancer… (more)

▼ The application of fluid shear stress on leukocytes and tumor cells in the circulation plays a critical role in the progression of inflammation and cancer metastasis, respectively. Specifically, fluid shear forces are known to help mediate selectin-based interactions between endothelial cells and circulating cells such as tumor cells and leukocytes, which can lead to their subsequent transmigration into tissues. However, how fluid shear forces induce mechanotransduction in circulating cells remains largely unknown, and could provide insight into potentially controlling pathological conditions such as inflammation and metastasis for therapeutic purposes. Herein, fluid forces are shown to exert control over how leukocytes respond to inflammatory agents found in the circulation. Leukocyte pre-exposure to fluid shear stress was found to suppress early leukocyte activation in the presence of the bacterial peptide fMLP, as indicated by reductions in selectin adhesion molecule shedding, integrin activation, and cell morphological changes. Conversely, leukocyte exposure can also increase leukocyte activation in the presence of platelet-activating factor, a molecule typically upregulated during vascular injury. Utilizing the same in vitro system, tumor cells became sensitized to the apoptosis-inducing ligand TRAIL in the presence of fluid shear stress conditions of the vasculature. This effect is not witnessed upon tumor cell treatment with the commonly utilized chemotherapeutic doxorubicin, which enacts its therapeutic effect via DNA intercalation. Results from this work suggest that TRAIL is well suited for systemic delivery, and that receptor-mediated apoptosis in general could be an ideal approach for circulating tumor cell therapies. The unique apoptotic effects of TRAIL in the presence of fluid shear stress were then exploited to develop a novel nanoparticle platform for therapeutic targeting of cancer cells in the circulation in vivo. Specifically, E-selectin functionalized liposomes were effective at rapidly targeting and adhering to cancer cells under shear stress conditions in the circulation, while also delivering therapeutic cargo. Utilizing both E-selectin and TRAIL, a nanoparticle platform was developed to functionalize circulating leukocytes of the bloodstream in attempt to neutralize circulating cancer cells. This approach, demonstrated in vitro with human blood and also in the circulation of mice in vivo, mimics the cytotoxic activity of natural killer cells and increases the surface area available for delivery of the receptor-mediated signal. The resulting "unnatural killer cells" hold promise as an effective means to neutralize circulating tumor cells that enter blood with the potential to form new metastases. Advisors/Committee Members: King, Michael R. (chair), Cerione, Richard A (committee member), Varner, Jeffrey D. (committee member).

Subjects/Keywords: Inflammation; Metastasis; Nanomedicine

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APA (6^th Edition):

Mitchell, M. (2014). Mechanotransduction And Therapeutic Targeting Of Cells In The Circulation. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/39384

Chicago Manual of Style (16^th Edition):

Mitchell, Michael. “Mechanotransduction And Therapeutic Targeting Of Cells In The Circulation.” 2014. Doctoral Dissertation, Cornell University. Accessed April 13, 2021. http://hdl.handle.net/1813/39384.

MLA Handbook (7^th Edition):

Mitchell, Michael. “Mechanotransduction And Therapeutic Targeting Of Cells In The Circulation.” 2014. Web. 13 Apr 2021.

Vancouver:

Mitchell M. Mechanotransduction And Therapeutic Targeting Of Cells In The Circulation. [Internet] [Doctoral dissertation]. Cornell University; 2014. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/1813/39384.

Council of Science Editors:

Mitchell M. Mechanotransduction And Therapeutic Targeting Of Cells In The Circulation. [Doctoral Dissertation]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/39384

Vanderbilt University

23. Stouch, Ashley Nicole. NF-kappa B signaling and inflammasome activation in developing fetal lung macrophages.

Degree: PhD, Cell and Developmental Biology, 2014, Vanderbilt University

URL: http://hdl.handle.net/1803/15353

► Bronchopulmonary dysplasia is a life-threatening lung disease affecting low birth weight preterm infants. While the occurrence of BPD is correlated with chorioamnionitis, the origination and… (more)

Subjects/Keywords: macrophage; inflammasome; inflammation

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APA (6^th Edition):

Stouch, A. N. (2014). NF-kappa B signaling and inflammasome activation in developing fetal lung macrophages. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/15353

Chicago Manual of Style (16^th Edition):

Stouch, Ashley Nicole. “NF-kappa B signaling and inflammasome activation in developing fetal lung macrophages.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed April 13, 2021. http://hdl.handle.net/1803/15353.

MLA Handbook (7^th Edition):

Stouch, Ashley Nicole. “NF-kappa B signaling and inflammasome activation in developing fetal lung macrophages.” 2014. Web. 13 Apr 2021.

Vancouver:

Stouch AN. NF-kappa B signaling and inflammasome activation in developing fetal lung macrophages. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/1803/15353.

Council of Science Editors:

Stouch AN. NF-kappa B signaling and inflammasome activation in developing fetal lung macrophages. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/15353

University of Bristol

24. Campbell, Jennie S. Investigating novel players in inflammatory cell migration to sites of tissue damage in vivo.

Degree: PhD, 2020, University of Bristol

URL: http://hdl.handle.net/1983/e5fb59ce-3715-4679-8113-97be14546369

► The use of model organisms is vital for the improvement of our understanding of dynamic immunological processes. Previous work in the developing Drosophila embryo has… (more)

▼ The use of model organisms is vital for the improvement of our understanding of dynamic immunological processes. Previous work in the developing Drosophila embryo has demonstrated that epithelial wounding by laser ablation induces the rapid production of hydrogen peroxide (H2O2). This early damage signal activates the tyrosine kinase Src42a within the embryonic hemocytes – the innate immune cells of the organism. Src42a subsequently phosphorylates the tissue damage receptor Draper on its intracellular immunoreceptor tyrosine activation motif (ITAM) domain. This recruits a second kinase – Shark – and results in the activation of hemocytes and their subsequent migration to the damage site. As kinase activation is key to the tissue damage response of these inflammatory cells, we reasoned that other hemocyte-specific proteins may also be phosphorylated following H2O2 signalling. Therefore, a phosphoproteomics screen was conducted in order to uncover novel H2O2/Src42a regulated phosphoproteins. Using this approach, we discovered a hemocyte wound recruitment defect in embryos lacking the PTP type phosphatase Pez. This was shown to be cell-autonomous; and time-lapse imaging revealed a lack of directionality within Pez mutant hemocytes in the presence of an epithelial wound. We also uncovered dynamic localisation of Pez in vivo and it’s colocalization with Draper during the engulfment of apoptotic debris. Finally, we demonstrated that the loss of Draper and Src42a leads to the mislocalisation of Pez. To investigate whether this signalling pathway is evolutionarily conserved, tail fin clipping of 3 dpf Danio rerio larvae was utilised. Excitingly, Draper orthologue (MEGF10) morphants showed a reduction in both neutrophil and macrophage numbers recruited to the wound margin. This observation was further confirmed by the generation transient CRISPant larvae. Finally, we demonstrated that the Pez orthologue – named PTPN21 – also plays a role in inflammation in the zebrafish following gene disruption by CRISPR.

Subjects/Keywords: Drosophila; Zebrafish; Inflammation

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APA (6^th Edition):

Campbell, J. S. (2020). Investigating novel players in inflammatory cell migration to sites of tissue damage in vivo. (Doctoral Dissertation). University of Bristol. Retrieved from http://hdl.handle.net/1983/e5fb59ce-3715-4679-8113-97be14546369

Chicago Manual of Style (16^th Edition):

Campbell, Jennie S. “Investigating novel players in inflammatory cell migration to sites of tissue damage in vivo.” 2020. Doctoral Dissertation, University of Bristol. Accessed April 13, 2021. http://hdl.handle.net/1983/e5fb59ce-3715-4679-8113-97be14546369.

MLA Handbook (7^th Edition):

Campbell, Jennie S. “Investigating novel players in inflammatory cell migration to sites of tissue damage in vivo.” 2020. Web. 13 Apr 2021.

Vancouver:

Campbell JS. Investigating novel players in inflammatory cell migration to sites of tissue damage in vivo. [Internet] [Doctoral dissertation]. University of Bristol; 2020. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/1983/e5fb59ce-3715-4679-8113-97be14546369.

Council of Science Editors:

Campbell JS. Investigating novel players in inflammatory cell migration to sites of tissue damage in vivo. [Doctoral Dissertation]. University of Bristol; 2020. Available from: http://hdl.handle.net/1983/e5fb59ce-3715-4679-8113-97be14546369

University of Newcastle

25. Berthon, Bronwyn. Investigating the link between corticosteroids and diet in adults with asthma.

Degree: PhD, 2014, University of Newcastle

URL: http://hdl.handle.net/1959.13/1051152

►

Research Doctorate - Doctor of Philosophy (PhD)

Asthma is public health problem, affecting adults and children of all ages globally. As there is no cure… (more)

▼

Research Doctorate - Doctor of Philosophy (PhD)

Asthma is public health problem, affecting adults and children of all ages globally. As there is no cure for asthma, optimum management of the condition is essential through appropriate pharmacotherapy and modification of environmental and lifestyle risk factors. Dietary intake and weight gain are important environmental exposures that may contribute to pathogenesis and progression of asthma, given the proposed association of asthma and obesity and evidence that some dietary nutrients affect asthma outcomes beneficially or adversely. Furthermore it is unknown whether asthma treatment medication, such as oral or inhaled corticosteroids impact upon dietary intake or cause weight gain and whether biological markers such as leptin are important in this association. Further investigation into these risk factors is required to improve asthma management. The current thesis aims to describe the dietary intake of adults with asthma; to investigate the association of dietary nutrient intake with corticosteroids and asthma outcomes; and to examine whether oral corticosteroids affect appetite, dietary intake, body weight and body composition in adults with asthma. Chapter 2 presents the current evidence for the effect of oral corticosteroids on appetite, dietary intake, body weight and body composition. In this systematic literature review we found it was unlikely that oral corticosteroids have a significant effect on dietary intake, appetite or body weight and composition when used to treat inflammatory conditions or in healthy subjects. There is limited objective evidence for the association of oral corticosteroids and these adverse effects, particularly with respect to short term oral corticosteroid therapy in inflammatory conditions, including asthma. In Chapter 3 the dietary intake of adults with asthma was examined; compared to healthy subjects; and evaluated for associations with biological markers and asthma outcomes. Subjects with severe asthma were found to have a different dietary intake to healthy subjects, with an increased intake of fat and sodium and decreased intake of fibre and potassium. In all subjects with asthma increased fat and decreased fibre intake were associated with greater airway inflammation and poorer lung function. This finding suggests that these nutrients may be important to address in nutritional counselling of adults with asthma. There was no relationship between dietary intake and inhaled or oral corticosteroids. Serum leptin was increased in subjects with asthma compared to healthy controls, and while it was not directly related to dietary intake, it was associated with inhaled corticosteroid use in males. This finding is an indication that leptin may be important to investigate further in the relationship between appetite and corticosteroid use in asthma. Chapter 4 explored the effects of a short term oral corticosteroid intervention on appetite, dietary intake, leptin, body weight and body composition in adults with asthma. This 10 day,…

Advisors/Committee Members: University of Newcastle. Faculty of Health & Medicine, School of Biomedical Sciences and Pharmacy.

Subjects/Keywords: asthma; diet; inflammation

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APA (6^th Edition):

Berthon, B. (2014). Investigating the link between corticosteroids and diet in adults with asthma. (Doctoral Dissertation). University of Newcastle. Retrieved from http://hdl.handle.net/1959.13/1051152

Chicago Manual of Style (16^th Edition):

Berthon, Bronwyn. “Investigating the link between corticosteroids and diet in adults with asthma.” 2014. Doctoral Dissertation, University of Newcastle. Accessed April 13, 2021. http://hdl.handle.net/1959.13/1051152.

MLA Handbook (7^th Edition):

Berthon, Bronwyn. “Investigating the link between corticosteroids and diet in adults with asthma.” 2014. Web. 13 Apr 2021.

Vancouver:

Berthon B. Investigating the link between corticosteroids and diet in adults with asthma. [Internet] [Doctoral dissertation]. University of Newcastle; 2014. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/1959.13/1051152.

Council of Science Editors:

Berthon B. Investigating the link between corticosteroids and diet in adults with asthma. [Doctoral Dissertation]. University of Newcastle; 2014. Available from: http://hdl.handle.net/1959.13/1051152

University of Toronto

26. Choi, So Jung. Effect of Remote Ischemic Conditioning on Lipopolysaccharide-induced Pulmonary Inflammation.

Degree: 2016, University of Toronto

URL: http://hdl.handle.net/1807/72691

►

Remote ischemic preconditioning (RIPC), an intervention whereby an extremity undergoes brief repeated cycles of ischemia/reperfusion (I/R), has been shown to exert protective effects on distant… (more)

Subjects/Keywords: Inflammation; leukocytes; 0564

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APA (6^th Edition):

Choi, S. J. (2016). Effect of Remote Ischemic Conditioning on Lipopolysaccharide-induced Pulmonary Inflammation. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/72691

Chicago Manual of Style (16^th Edition):

Choi, So Jung. “Effect of Remote Ischemic Conditioning on Lipopolysaccharide-induced Pulmonary Inflammation.” 2016. Masters Thesis, University of Toronto. Accessed April 13, 2021. http://hdl.handle.net/1807/72691.

MLA Handbook (7^th Edition):

Choi, So Jung. “Effect of Remote Ischemic Conditioning on Lipopolysaccharide-induced Pulmonary Inflammation.” 2016. Web. 13 Apr 2021.

Vancouver:

Choi SJ. Effect of Remote Ischemic Conditioning on Lipopolysaccharide-induced Pulmonary Inflammation. [Internet] [Masters thesis]. University of Toronto; 2016. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/1807/72691.

Council of Science Editors:

Choi SJ. Effect of Remote Ischemic Conditioning on Lipopolysaccharide-induced Pulmonary Inflammation. [Masters Thesis]. University of Toronto; 2016. Available from: http://hdl.handle.net/1807/72691

27. Al-Rifai, Sarah. Rôle de la résistine hypothalamique dans l'installation de l’inflammation hypothalamique et l’insulino-résistance : impact de la consommation aigüe ou chronique d'un régime hyper lipidique : Role of hypothalamic resistin in the onset of hypothalamic inflammation and insulin resistance : impact of acute or chronic high fat diet consumption.

Degree: Docteur es, Aspects moléculaires et cellulaires de la biologie, 2019, Université Paris-Saclay (ComUE)

URL: http://www.theses.fr/2019SACLS095

► La prévalence de l’obésité est en net progrès et constitue un problème majeur de santé publique. Cette pathologie est d’autant plus dangereuse qu’elle s’accompagne d’un… (more)

▼ La prévalence de l’obésité est en net progrès et constitue un problème majeur de santé publique. Cette pathologie est d’autant plus dangereuse qu’elle s’accompagne d’un cluster de désordres métaboliques dont l’inflammation chronique de bas grade et la résistance à l’insuline, principal facteur de risque du diabète de type 2. Les études montrent que la consommation d’un régime hyper lipidique (HFD) représente la cause majeure qui expose à l’obésité et aux pathologies qui lui sont associées. L’obésité induite par un régime HFD s’associe en effet à une inflammation hypothalamique ainsi qu’une altération des circuits neuronaux régissant le contrôle de la balance énergétique, ces altérations sont propices aux développements de résistances à l’insuline et à la leptine. De récentes études montrent que la consommation d’un régime HFD de quelques jours seulement s’accompagne d’une inflammation hypothalamique transitoire, antérieure à l’installation de l’obésité et à l’inflammation périphérique. Ces résultats suggèrent que l’inflammation hypothalamique précoce représente une étape critique dans le développement de l’obésité et de ses altérations. Les médiateurs et les voies de signalisations impliqués dans l’installation de l’inflammation hypothalamique ne sont pas totalement élucidées. Chez les rongeurs, la résistine est associée à l’inflammation et l’insulino-résistance au cours de l’obésité. Bien que majoritairement produite par le tissu adipeux, les études montrent que la résistine est également exprimée par l’hypothalamus ; toutefois, peu d’études renseignent sur son action au niveau central. Notre équipe a démontré chez le rat, qu’une perfusion centrale de résistine altère fortement la sensibilité à l’insuline via l’activation du récepteur TLR4 et l’induction des principales voies de l’inflammation. Dans ce contexte, l’objectif de cette étude a été d’investiguer le rôle de la voie résistine/TLR4 dans l’installation de l’inflammation hypothalamique associée au régime HFD. Nous montrons pour la première fois que, chez la souris, la consommation d’un régime HFD provoque une augmentation de l’expression génique de la résistine dans l’hypothalamus dès 3 jours de régime HFD. L’expression de la résistine est diminuée jusqu’au niveau basal après 8 jours et est de nouveau fortement augmentée après 8 semaines de régime HFD. Nous montrons que l’augmentation de l’expression de la résistine est concomitante avec la gliose réactionnelle associée au régime HFD de court terme, connue pour précocement altérer l’équilibre de la balance énergétique. De façon intéressante, nous montrons quel’augmentation de l’expression de la résistine est observée dans les neurones anorexigènes POMC, critiques pour le maintien de l’homéostasie énergétique ainsi que dans les tanycytes dont les prolongements contactent les capillaires fenêtrés du sang porte hypothalamohypophysaire et dont l’importance pour l’équilibre de la balance énergétique a été démontrée. De façon intéressante, nous montrons que la résistine active l’inflammation dans les tanycytes via… Advisors/Committee Members: Taouis, Mohammed (thesis director).

Subjects/Keywords: Résistine; Inflammation; Insulino-Résistance; Diabète; Inflammation; Obésité; Resistin; Inflammation; Insulin resistance; Diabetes; Inflammation; Obesity

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APA (6^th Edition):

Al-Rifai, S. (2019). Rôle de la résistine hypothalamique dans l'installation de l’inflammation hypothalamique et l’insulino-résistance : impact de la consommation aigüe ou chronique d'un régime hyper lipidique : Role of hypothalamic resistin in the onset of hypothalamic inflammation and insulin resistance : impact of acute or chronic high fat diet consumption. (Doctoral Dissertation). Université Paris-Saclay (ComUE). Retrieved from http://www.theses.fr/2019SACLS095

Chicago Manual of Style (16^th Edition):

Al-Rifai, Sarah. “Rôle de la résistine hypothalamique dans l'installation de l’inflammation hypothalamique et l’insulino-résistance : impact de la consommation aigüe ou chronique d'un régime hyper lipidique : Role of hypothalamic resistin in the onset of hypothalamic inflammation and insulin resistance : impact of acute or chronic high fat diet consumption.” 2019. Doctoral Dissertation, Université Paris-Saclay (ComUE). Accessed April 13, 2021. http://www.theses.fr/2019SACLS095.

MLA Handbook (7^th Edition):

Al-Rifai, Sarah. “Rôle de la résistine hypothalamique dans l'installation de l’inflammation hypothalamique et l’insulino-résistance : impact de la consommation aigüe ou chronique d'un régime hyper lipidique : Role of hypothalamic resistin in the onset of hypothalamic inflammation and insulin resistance : impact of acute or chronic high fat diet consumption.” 2019. Web. 13 Apr 2021.

Vancouver:

Al-Rifai S. Rôle de la résistine hypothalamique dans l'installation de l’inflammation hypothalamique et l’insulino-résistance : impact de la consommation aigüe ou chronique d'un régime hyper lipidique : Role of hypothalamic resistin in the onset of hypothalamic inflammation and insulin resistance : impact of acute or chronic high fat diet consumption. [Internet] [Doctoral dissertation]. Université Paris-Saclay (ComUE); 2019. [cited 2021 Apr 13]. Available from: http://www.theses.fr/2019SACLS095.

Council of Science Editors:

Al-Rifai S. Rôle de la résistine hypothalamique dans l'installation de l’inflammation hypothalamique et l’insulino-résistance : impact de la consommation aigüe ou chronique d'un régime hyper lipidique : Role of hypothalamic resistin in the onset of hypothalamic inflammation and insulin resistance : impact of acute or chronic high fat diet consumption. [Doctoral Dissertation]. Université Paris-Saclay (ComUE); 2019. Available from: http://www.theses.fr/2019SACLS095

University of Waikato

28. Newland, Julia. In vitro cell culture to study microglial inflammation .

Degree: 2016, University of Waikato

URL: http://hdl.handle.net/10289/12053

► Inflammation of the central nervous system (CNS) characterised by release of cytokines such as tumour necrosis factor-alpha (TNF-a) and interleukin-1 (IL-1) is an event that… (more)

▼ Inflammation of the central nervous system (CNS) characterised by release of cytokines such as tumour necrosis factor-alpha (TNF-a) and interleukin-1 (IL-1) is an event that is often detrimental to neuronal cells and is thought to contribute to the neuronal loss observed during neurodegeneration. One objective of this study was to investigate the potential anti-inflammatory properties of kawakawa leaf extracts using in vitro model cell systems. Kawakawa leaf extracts anti-inflammatory properties have anecdotally been documented in traditional Maori medicinal practices (Rangoa). However, before this aspect could be carried out, experiments were undertaken to investigate the effects the kawakawa leaf extracts had on the growth rates of two mammalian cell lines (HeLa and THP-1 cells). Interestingly, the growth assays showed that the extracts to have both a stimulatory and inhibitory effect on cell growth. Toxicity of cells can be categorised as either necrotic or apoptotic cell death. In this study, HeLa cells and THP-1 cells were incubated under standard growth conditions with various concentrations (10 to 100ug/ml) of Kawakawa leave extracts prepared at room temperature or 60OC. Growth data as seen in figures 2 and 3 typically have a long lag phase before they start to reach exponential growth between days 4 and 5. The extract having the largest stimulatory effect on HeLa cells as shown by figure 6 was 25 ug/ml at 60OC and the largest inhibitory effect seen on HeLa cells was seen at 50 ug/ml RT shown by figure 6. The extract which has the largest stimulatory effect on THP-1 cells is 25 ug/ml 60OC as shown by figure 11 whereas the extract producing the largest inhibitory effect is 25 ug/ml RT. Apoptotic and necrotic cell death mechanisms were examined by using in vitro biochemistry techniques. Assessments were largely made based on biochemical changes of HeLa cells and THP-1 cells post treatment of Kawakawa leave extracts. Measurement of lactate dehydrogenase (LDH assays) in the growth media of cells that were shown to be growth inhibited during exposure to Kawakawa extracts indicated that the growth inhibition resulting from exposure to the extracts was not due to necrotic cell death processes. (ie that cells maintained their membrane integrity) When compared to the control, a lower amount of cytosolic LDH was seen in THP-1 cell lines. However, HeLa cell lines produced a high level of cytosolic LDH which may be due to mycoplasma contamination. On average, Kawakawa concentrations at 12.5ug/ml and 25ug/ml yielded less lysed cells percentage across both cell lines. The demonstrated cell growth inhibition was unlikely to be due to necrosis and because of this it was decided to see if cell death was caused by mitochondrial processes that would further support apoptotic cell death. The biochemical assay MTT indirectly measures mitochondrial dehydrogenase activity in the presence of kawakawa leave extracts. The MTT data illustrated mitochondrial impairment where HeLa cells exposed to Kawakawa 60OC concentrations… Advisors/Committee Members: Martinus, Ryan Dennis (advisor).

Subjects/Keywords: CNs; inflammation; Microglial

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

APA (6^th Edition):

Newland, J. (2016). In vitro cell culture to study microglial inflammation . (Masters Thesis). University of Waikato. Retrieved from http://hdl.handle.net/10289/12053

Chicago Manual of Style (16^th Edition):

Newland, Julia. “In vitro cell culture to study microglial inflammation .” 2016. Masters Thesis, University of Waikato. Accessed April 13, 2021. http://hdl.handle.net/10289/12053.

MLA Handbook (7^th Edition):

Newland, Julia. “In vitro cell culture to study microglial inflammation .” 2016. Web. 13 Apr 2021.

Vancouver:

Newland J. In vitro cell culture to study microglial inflammation . [Internet] [Masters thesis]. University of Waikato; 2016. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10289/12053.

Council of Science Editors:

Newland J. In vitro cell culture to study microglial inflammation . [Masters Thesis]. University of Waikato; 2016. Available from: http://hdl.handle.net/10289/12053

University of Manchester

29. Ince, Louise. Circadian rhythms in glucocorticoid signalling and pulmonary inflammation.

Degree: 2015, University of Manchester

URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:260799

► The circadian clock drives ~24hr rhythms in a variety of processes, from gene expression through to behaviour, facilitating anticipation of daily changes in the external… (more)

▼ The circadian clock drives ~24hr rhythms in a variety of processes, from gene expression through to behaviour, facilitating anticipation of daily changes in the external environment and temporal separation of internal processes. This pacemaker is a critical regulator of immune function and many inflammatory diseases show time-of-day variation in symptom severity. Disruption of the pacemaker by manipulation of the daily cycle of light and dark exposure (experimental ‘jet lag’) is known to exacerbate inflammatory responses to innate immune challenge, and recent evidence has highlighted immuno-modulatory roles for components of the molecular oscillator in peripheral tissues. The adrenal-derived glucocorticoid hormones are potent anti-inflammatory molecules and are capable of modulating circadian oscillations in peripheral tissues. This, along with their rhythmic secretion profile, makes them key candidates as mediators of circadian regulation of inflammatory signalling.Utilising adrenalectomy, timed glucocorticoid administration, hormone clamp and genetic targeting of the glucocorticoid receptor in mice, I present evidence for an interaction between glucocorticoid signalling and the circadian pacemaker in regulating the pulmonary inflammatory response to lipopolysaccharide (LPS) challenge. The neutrophilic response to aerosolised LPS exhibits a clear time-of-day effect in vivo, which is lost after disruption of endogenous glucocorticoid production via adrenalectomy. However, replacement of a rhythmic circulating glucocorticoid concentration with a flat daily average using a subcutaneous hormone clamp does not disrupt the inflammatory rhythm. Finally, a novel mouse strain was produced with disrupted expression of the glucocorticoid receptor (GR) in bronchial epithelial cells (Ccsp-GR-/-). These cells are critical regulators of circadian rhythmicity in the lung and drive rhythmic neutrophil influx in response to LPS stimulation through production of the chemokine CXCL5. Loss of GR in the bronchial epithelium was associated with a loss of rhythmic neutrophil influx after challenge, but anti-inflammatory sensitivity to the synthetic glucocorticoid dexamethasone remained.Collectively, these data show that appropriate temporal modulation of pulmonary inflammation requires functional glucocorticoid signalling, although the ligand itself does not need to oscillate. The retention of anti-inflammatory dexamethasone sensitivity suggests a role for cross-talk between the bronchial epithelium and additional cell populations, consistent with recent evidence for immuno-suppressive macrophage-epithelium communication in the lung. These are the first studies to dissect the mechanistic links between clocks, glucocorticoids and immunological responses in a target tissue. Advisors/Committee Members: RAY, DAVID DW, GIBBS, JULIE JE, Ray, David, Gibbs, Julie, Loudon, Andrew.

Subjects/Keywords: Circadian; Inflammation; Glucocorticoids

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

APA (6^th Edition):

Ince, L. (2015). Circadian rhythms in glucocorticoid signalling and pulmonary inflammation. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:260799

Chicago Manual of Style (16^th Edition):

Ince, Louise. “Circadian rhythms in glucocorticoid signalling and pulmonary inflammation.” 2015. Doctoral Dissertation, University of Manchester. Accessed April 13, 2021. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:260799.

MLA Handbook (7^th Edition):

Ince, Louise. “Circadian rhythms in glucocorticoid signalling and pulmonary inflammation.” 2015. Web. 13 Apr 2021.

Vancouver:

Ince L. Circadian rhythms in glucocorticoid signalling and pulmonary inflammation. [Internet] [Doctoral dissertation]. University of Manchester; 2015. [cited 2021 Apr 13]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:260799.

Council of Science Editors:

Ince L. Circadian rhythms in glucocorticoid signalling and pulmonary inflammation. [Doctoral Dissertation]. University of Manchester; 2015. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:260799

University of Ottawa

30. Ametepe, Sandra Emmanuelle. FoxO3a Signaling Promotes the Inflammatory Response During Salmonella Typhimurium Infection .

Degree: 2017, University of Ottawa

URL: http://hdl.handle.net/10393/35865

► FoxO3a is a transcription factor that regulates various cellular functions such as cell cycle or cell death. However, its role in the innate immune response… (more)

Subjects/Keywords: FoxO3a; Salmonella; Inflammation

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

APA (6^th Edition):

Ametepe, S. E. (2017). FoxO3a Signaling Promotes the Inflammatory Response During Salmonella Typhimurium Infection . (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/35865

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):

Ametepe, Sandra Emmanuelle. “FoxO3a Signaling Promotes the Inflammatory Response During Salmonella Typhimurium Infection .” 2017. Thesis, University of Ottawa. Accessed April 13, 2021. http://hdl.handle.net/10393/35865.

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

MLA Handbook (7^th Edition):

Ametepe, Sandra Emmanuelle. “FoxO3a Signaling Promotes the Inflammatory Response During Salmonella Typhimurium Infection .” 2017. Web. 13 Apr 2021.

Vancouver:

Ametepe SE. FoxO3a Signaling Promotes the Inflammatory Response During Salmonella Typhimurium Infection . [Internet] [Thesis]. University of Ottawa; 2017. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10393/35865.

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

Council of Science Editors:

Ametepe SE. FoxO3a Signaling Promotes the Inflammatory Response During Salmonella Typhimurium Infection . [Thesis]. University of Ottawa; 2017. Available from: http://hdl.handle.net/10393/35865

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

Open Access Theses and Dissertations