Dissertation (Ph.D.) -- University of Texas Southwestern Medical Center at Dallas, 2006. / Vita. Bibliography: p.148-174

Thesis (M.S.)--University of Missouri--Columbia, 2004. / "May 2004." Typescript. Includes bibliographical references (leaves 97-111). Also issued on the Internet.

Thesis (M.Sc.)--University of Alberta, 2010. / A thesis submitted to the Faculty of Graduate Studies and Research in partial fulfillment of the requirements for the degree of Master of Science in Physiology. Title from pdf file main screen (viewed on February 16, 2010). Includes bibliographical references.

Thesis (Ph. D.)--Ohio State University, 2009. / Title from first page of PDF file. Includes vita. Includes bibliographical references (p. 139-156).

Orientadores: Silvana Pereira Barros, Sergio Roberto Peres Line / Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba / Made available in DSpace on 2018-08-04T03:46:37Z (GMT). No. of bitstreams: 1 Vasconcelos_DanielFernandoPereira_M.pdf: 718453 bytes, checksum: 33e7ea7787a27dcce6c7a1cac2b7b5ed (MD5) Previous issue date: 2005 / Resumo: A doença periodontal (DP) é causada por interações entre fatores do hospedeiro, microrganismos específicos patogênicos e o sistema imunológico. TNF-b é um imunoregulador multifuncional que está relacionado com a patogênese de diversas desordens imunológicas, incluindo a DP. Nosso estudo analisou a associação entre DP e polimorfismo no gene TNF-b (+252 A/G). O DNA foi extraído de células da mucosa oral de 126 indivíduos brancos: 44 indivíduos controle e 82 indivíduos com DP. O polimorfismo foi analisado pela técnica de PCR, seguida pela RFLP. Os dados foram estatisticamente analisados pelo teste Exato Fisher (p<0,05) e Odds Ratio (OR). A freqüência do polimorfismo mostrou diferença estatisticamente significativa entre os grupos controle e com DP, revelando que indivíduos portadores do alelo G apresentavam 2,6 vezes mais chances de desenvolver a DP do que indivíduos saudáveis (G vs. A, p=0.0019, OR= 2.67, 95% CI 1.45 - 4.78), em relação aos genótipos a presença de pelo menos um alelo G predispõe 3,1 vezes à DP (G/G+ G/A vs. A/A, p=0,0059, OR= 3.1, 95% CI 1.45 - 6.65). Conclui-se que o TNF-b está envolvido na patogênese da periodontite crônica e pode ser utilizado como um marcador de risco para a DP na população estudada / Abstract: Background: Periodontitis is an inflammatory disease that leads to irreversible attachment loss, bone destruction and eventually bone loss, such cascade that culminates in tissue destruction initiates with pathogenic micro-organisms and depends on host response to disease expression. Tumor necrosis factor (TNF) a potent multifunctional immune modulator has been implicated in the pathogenesis of periodontal disease. Objective: In this study we investigated the hypothesis of association between chronic periodontitis (CP) and polymorphisms of the TNF-ß gene. Materials and Methods: One hundred twenty six individuals were evaluated by measuring clinical attachment loss and divided in 44 health individuals (control group-CG) and 82 subjects with CP. DNA samples were obtained from the individual's epithelial cells through scraping of the buccal mucosa. Polymorphism in the TNF-ß gene was analyzed by PCR, followed by NcoI restriction endonuclease digestion (RFLP). Results: The TNF-ß (+252A/G) polymorphism showed association with chronic periodontitis. Significant differences were found for the TNF-ß allele or carriage rate frequencies; odds ratio (OR)=2.67. Conclusions: These findings suggest that genotype composed of TNF- ß gene polymorphism may influence the susceptibility to chronic periodontitis / Mestrado / Histologia e Embriologia / Mestre em Biologia Buco-Dental

Please read the abstract in the section 00front of this document / Canine babesiosis, caused by the tick-borne protozoan Babesia canis rossi, is an economically important and potentially fatal disease of dogs in South Africa. The host's response to many infectious diseases is mediated (at least in part) by intercellular messengers called cytokines. One of the most important cytokines released is tumour necrosis factor (TNF). A study was designed to measure serum concentrations of TNF in dogs naturally infected with canine babesiosis and to relate TNF concentrations to clinical severity, mortality, rectal temperature and parasitaemia. There was a statistically significant difference in TNF concentrations between groups of differing disease severity, with a general trend of increasing mean 10g(TNF) with increasing severity of disease. A noteworthy finding was that dogs with hypoglycaemia had very high TNF (mean 15.03 nglml compared to a mean of 2.32 nglml for other sick dogs without hypoglycaemia). When TNF values were compared between survival and non-survival groups, there was no significant difference. The rectal temperature of the dogs in this study did not show any statistically significant association with TNF concentrations. When parasitaemia and TNF were examined within groups of infected dogs, there was no significant relationship. However, when the sample size was increased by pooling all infected dogs and treating them as a single group, there was a highly significant positive correlation (p = 0.003) between parasitaemia and serum TNF concentrations. The results ofthis study were encouraging and indicate that canine babesiosis may share a similar pathophysiology with human malaria in terms ofTNF being associated with disease severity. One ofthe most significant findings in this study was the presence ofvery high TNF values in two ofthree dogs with hypoglycaemia. Hypoglycaemia has not been previously recorded in dogs with babesiosis and is a potentially important finding particularly in view ofthe hypoglycaemia associated with malaria in humans. Malarial hypoglycaemia is correlated with a higher mortality in humans, especially in pregnant women and children. If the findings ofthis study can be Vl confinned and expanded, they may lend further support to the use of canine babesiosis as a model for some ofthe problems encountered in human malaria research. / Dissertation (MMed Vet (Med))--University of Pretoria, 2001. / Companion Animal Clinical Studies / unrestricted

The gut microbiota and its metabolites – namely short chain fatty acids (SCFAs) – interact with the digestive, immune, and nervous systems. Microbiota with disrupted composition are highly associated with obesity, gastrointestinal symptoms, and chronic inflammation. Levels of SCFAs in the feces can represent dynamics of the microbiota, and they represent one mechanism by which the microbiota interacts with its host. This study aimed to further our understanding of associations between microbiota bacterial diversity and SCFAs, immune markers, BMI, and GI symptoms and to identify bacteria that are differentially abundant in different BMI groups and with synbiotic supplementation. Data (SCFAs, immunoglobulins, body mass index, fecal fiber, fecal protein, measures of GI symptoms, and 16s RNA sequences, n=11) was extracted from a randomized control trial investigating the effects of synbiotic supplementation in non-celiac gluten-sensitive participants. QIIME2 was used to process 16s RNA data, analyze quantitative, qualitative, phylogenetic quantitative, and phylogenetic qualitative measures of alpha and beta diversity and to perform an analysis of composition of microbiomes (ANCOM) for identification of differential abundances. Multiple metrics of alpha diversity were found to significantly correlate with IgG4, IgM, IL-2, acetate, propionate, isobutyrate, valerate, isovalerate, caproate, heartburn, urgent need to defecate, and feelings of incomplete evacuation. Multiple metrics of beta diversity were significantly different between normal and overweight, normal and obese, and overweight and obese BMI classification groups. Beta diversity was also found to significantly correlate with IgG1, IgG3, IgG4, IgA, IL-6, IL-8, fecal fiber, propionate, butyrate, heartburn, acid regurgitation, nausea and vomiting, bloating, abdominal distension, increased gas, and eructation. The synbiotic intervention did not significantly alter alpha or beta diversity. An ANCOM identified bacterial taxa differentially abundant with BMI shifts and synbiotic supplementation, though these taxa were not those included in the synbiotic. Findings demonstrate alpha and beta diversity associations with various SCFAs, GI symptoms, immune markers, and BMI, and the results of the placebo-controlled intervention suggest careful consideration of placebo contents moving forward. This research supports plans to apply analysis to larger sample sizes to elucidate changes microbial profiles that are associated with clinically relevant biomarkers and symptoms.

The ability of fungal-derived β-glucan particles to induce leukocyte activation and the production of inflammatory mediators, such as tumor necrosis factor (TNF)-α, is a well characterized phenomenon. Although efforts have been made to understand how these carbohydrate polymers exert their immunomodulatory effects, the receptors involved in generating these responses are unknown. Here we show that Dectin-1 mediates the production of TNF-α in response to zymosan and live fungal pathogens, an activity that occurs at the cell surface and requires the cytoplasmic tail and immunoreceptor tyrosine activation motif of Dectin-1 as well as Toll-like receptor (TLR)-2 and Myd88. This is the first demonstration that the inflammatory response to pathogens requires recognition by a specific receptor in addition to the TLRs. Furthermore, these studies implicate Dectin-1 in the production of TNF-α in response to fungi, a critical step required for the successful control of these pathogens.

No description available.

Tsoi Lo Ming. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2006. / Includes bibliographical references (leaves 99-109). / Abstracts in English and Chinese. / Acknowledgements --- p.I / Abstract --- p.II / Abstract in Chinese --- p.III / List of Abbreviations --- p.IV / List of Figures --- p.V / List of Tables --- p.VI / Table of Contents --- p.VII / Chapter Chapter 1 : --- Introduction / Chapter 1.1. --- Apolipoprotein and Lipoprotein Metabolism --- p.1 / Chapter 1.2. --- Molecular Information of ApoE --- p.2 / Chapter 1.3. --- Tissue Distribution of ApoE --- p.2 / Chapter 1.4. --- Functions of ApoE --- p.4 / Chapter 1.5. --- Genetic Polymorphism of ApoE --- p.7 / Chapter 1.6. --- Protein Structure and Characteristics of ApoE Isoforms --- p.9 / Chapter 1.7. --- Plasma and Cellular Expression Level of ApoE Isoforms --- p.12 / Chapter 1.8. --- Association between ApoE Isoforms and Plasma Lipid Profiles --- p.13 / Chapter 1.9. --- ApoE Polymorphisms and Pathophysiological Conditions / Chapter 1.9.1. --- Type III Hyperlipoproteinemia (Type III HLP) --- p.14 / Chapter 1.9.2. --- Alzheimer's Disease --- p.15 / Chapter 1.9.3. --- Atherosclerosis / Chapter 1.9.3.1. --- Atherosclerosis - An Inflammatory Process --- p.15 / Chapter 1.9.3.2. --- Role of ApoE in Atherosclerosis --- p.18 / Chapter (a) --- Functions Associated to Lipid Metabolism --- p.19 / Chapter (b) --- Functions Independent to Lipid Metabolism --- p.20 / Chapter 1.9.3.3. --- TNF-α and IL-6 in Atherosclerosis --- p.25 / Chapter 1.10. --- Macrophage Cytokine Expression and MAPKs / Chapter 1.10.1. --- Organization of MAPKs Signaling Pathway --- p.26 / Chapter 1.10.2. --- Lipopolysaccharide and MAPKs in Macrophage Cytokine Expression --- p.28 / Chapter 1.10.3. --- Regulation of Macrophage Cytokine Expression / Chapter 1.10.3.1. --- ERK1/2 and p38 MAPK Pathway --- p.30 / Chapter 1.10.3.2. --- Arachidonic Acid Metabolism --- p.30 / Chapter 1.11. --- Aim and Hypothesis --- p.31 / Chapter Chapter 2 : --- Materials and Methods / Materials / Chapter 2.1 --- Culture of ApoE-isoform-expressing J774A.1 Macrophage Cell Line --- p.32 / Chapter 2.2 --- RNA Extraction and Reverse Transcription-Polymerase Chain Reaction (RT-PCR) --- p.33 / Chapter 2.3 --- Protein Extraction and Quantification --- p.37 / Chapter 2.4 --- Enzyme-linked Immunosorbent Assay (ELISA) --- p.38 / Chapter 2.5 --- Western Blotting --- p.39 / Chapter 2.6 --- LPS Treatment --- p.42 / Chapter 2.7 --- MAPK Inhibitor Experiment --- p.43 / Methods / Chapter 2.8 --- Study on the Effect of Endogenously Expressed ApoE Isoforms on Macrophage Cytokine Secretion / Chapter 2.8.1. --- Establishment of ApoE-isoform-expressing Macrophages --- p.44 / Chapter 2.8.2. --- Semi-quantification of ApoE mRNA Level by RT-PCR / Chapter 1) --- Isolation of Total RNA --- p.45 / Chapter 2) --- RT-PCR --- p.46 / Chapter 2.8.3. --- Determination of ApoE Protein Expression Level by ELISA and Western Blot --- p.47 / Chapter 1) --- Quantification of Total Proteins --- p.48 / Chapter 2) --- ELISA --- p.48 / Chapter 3) --- Western Blot --- p.49 / Chapter 2.8.4. --- LPS Treatment --- p.51 / Chapter 2.8.5. --- MEK1/2 Inhibitor Experiment --- p.53 / Chapter 2.8.6. --- p38 Inhibitor Experiment --- p.54 / Chapter 2.9 --- Study on the Effect of Exogenous ApoE Isoform on Macrophage Cytokine Secretion --- p.55 / Chapter 2.10 --- Statistical Analysis --- p.55 / Chapter Chapter 3: --- Results / Changes of Inflammatory Properties Associated with Endogenous ApoE Isoform Expression in Macrophages / Chapter 3.1 --- Characterization of ApoE-isoform-expressing Macrophages --- p.56 / Chapter 3.1.1. --- Cell Lines with Stable Expression of ApoE Isoforms --- p.56 / Chapter 3.2 --- Cell Morphology Study --- p.58 / Chapter 3.3 --- Changes of IL-6 and TNF-α Secretion Associated with Endogenous ApoE Isoforms Expression / Chapter 3.3.1. --- In the Presence of Lipoproteins --- p.60 / Chapter 3.3.2. --- Serum/Lipoprotein-independent Effects of ApoE Isoforms --- p.63 / Chapter 3.4 --- The Effects of Endogenous ApoE Isoform Expression on the Activities of MAPK Signaling Pathways / Chapter 3.4.1. --- Study on the Activation Status and Expression of MAPKs --- p.66 / Chapter 1) --- ERK1/2 MAPK Pathway --- p.66 / Chapter 2) --- p38 MAPK Pathway --- p.69 / Chapter 3.4.2. --- IL-6 and TNF-a Secretion Among ApoE Isoforms in the Presence of MEK1/2 mhibitor --- p.72 / Chapter 3.4.3. --- IL-6 and TNF-α Secretion Among ApoE Isoforms in the Presence of p38 Inhibitor --- p.75 / Chapter Chapter 4 : --- Discussions / Chapter 4.1. --- Mouse Peritoneal Macrophage Cell Line J774A.1 as Cell Model --- p.79 / Chapter 4.2. --- Inflammatory Properties Associated with Endogenous ApoE Isoform Expression in Macrophages / Chapter 4.2.1. --- Expression Level of ApoE Isoform Transgenes in Mouse Peritoneal Macrophages --- p.80 / Chapter 4.2.2. --- Macrophage Activation by LPS --- p.81 / Chapter 4.2.3. --- Effect of Endogenous ApoE Isoform Expression on Cytokine Secretion and Signal Transduction in Macrophages --- p.82 / Chapter 4.3. --- Conclusions and Future Prospects / Chapter 4.3.1. --- Conclusions --- p.90 / Chapter 4.3.2. --- Future Prospects --- p.91 / Chapter Chapter 5 : --- Appendices / Chapter 5.1 --- Changes of Inflammatory Properties of Macrophages Supplemented with Exogenous ApoE Isoforms / Chapter 5.1.1. --- Changes of IL-6 and TNF-a Secretion in Macrophages Supplemented with Exogenous ApoE Isoforms --- p.92 / Chapter 5.1.2. --- Changes of Signal Transduction in Macrophages Supplemented with Exogenous ApoE Isoforms / Chapter 5.1.2.1. --- Study on the Activation Status and Expression of MAPKs / Chapter 1) --- ERK1/2 MAPK Pathway --- p.95 / Chapter 2) --- p38 MAPK Pathway --- p.97 / Chapter Chapter 6: --- Bibliography --- p.99