Academic literature on the topic '3204 Immunology'
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Journal articles on the topic "3204 Immunology"
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Zeisberg, Michael. "Fibroblasts emerge via epithelial-mesenchymal transition in chronic kidney fibrosis." Frontiers in Bioscience Volume, no. 13 (2008): 6991. http://dx.doi.org/10.2741/3204.
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Heo, J., and T. Park. "Abstract # 3204 Neuroprotective effects of TNF-alpha inhibitor on rat hippocampal organotypic slice cultures treated with the 1-42 beta–amyloid." Brain, Behavior, and Immunity 81 (October 2019): 1. http://dx.doi.org/10.1016/j.bbi.2019.08.011.
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Cano Garcia, L., S. Manrique Arija, F. Godoy-Navarrete, A. M. Cabezas-Lucena, G. Diaz-Cordobes, and N. Mena-Vázquez. "AB0865-HPR FREQUENCY OF DEPRESSION IN SYSTEMIC LUPUS ERYTHEMATOSUS." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 1456.2–1456. http://dx.doi.org/10.1136/annrheumdis-2021-eular.3204.
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Objectives:Cross-sectional observational study of a series of SLE patients selected from the Rheumatology consultations.Methods:age ≥18 years with SLE (ACR 1997 criteria) capable of understanding and willing to take the questionnaires. Protocol: All patients with SLE undergoing follow-up in the rheumatology clinic are recorded in a database. A telephone call was made to all the patients included in the database and those patients who responded to the call and gave their verbal consent for the collection of data from their clinical history and completed the Goldberg questionnaire were finally included. The nurse was in charge of explaining the questionnaire to the patients. Variables: the main outcome variable was depression assessed by Goldberg (≥2 depression) and other variables were: previous diagnosis of depression, Charlson index, polypharmacy, psychiatric medication, referral to mental health or primary care, SLEDAI and SLICC. Descriptive, bivariate statistical analysis and multivariate logistic regression analysis (VD: Goldberg depression).Results:89 patients with SLE were included (95.5% women, mean age 49.44 ± 13.2 years and 18.28 ± 9.19 years of disease). The mean (SD) of the Goldberg scale in all the patients was 3.2 ± 2.9 and a total of 45 patients (50.4%) met criteria of depression according to Goldberg’s screening, of which 19 (21.3%) patients had a previous diagnosis of depression. Only 9 patients (10.1%) had had a mental health follow-up and 22 patients (24.7%) were being followed by the family doctor. A total of 87 patients (97.8%) presented polypharmacy: severe polypharmacy 59 (66.3%) and 33 (37.1%) psychiatric medication. The most used psychiatric medication was: 7 (7.8%) bromazepam, 6 (6.7%) citalopram, 5 (5.6%) diazepam. Regarding comorbidities, the Charlson index was 1.82 ± 1.21, also highlighting that 34 (27%) of the sample had Sjögren syndrome. In the multivariate analysis, polypharmacy (OR, 1.8 [95% CI, 1.0-3.1]) and Sjogren’s syndrome (OR, 3.8 [95% CI, 1.0-10.7]) were independently associated with depression by Goldberg.Conclusion:Depression is underdiagnosed and undertreated in patients with SLE. Depression is associated with polypharmacy and the perception of patients with SLE of being ill. It is important to correctly treat depression in the context of SLE comorbidity due to its great impact on quality of life.Disclosure of Interests:None declared
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van den Hombergh, W., M. van der Burgt, F. van den Hoogen, J. Fransen, and M. Vonk. "FRI0508 Type and Timing of First Symptoms in Systemic Sclerosis: Prediction of Disease Course: Table 1." Annals of the Rheumatic Diseases 73, Suppl 2 (June 2014): 571.2–571. http://dx.doi.org/10.1136/annrheumdis-2014-eular.3204.
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Moltό, A., H. Bachelez, K. Dawidowicz, D. Wendling, G. Hayem, F. Lioté, F. Aubin, A. Nassif, M. Viguier, and P. Richette. "SAT0257 Is hidradenitis suppurativa an extra articular feature of spondyloarthritis? Results from a multicentre national prospective study." Annals of the Rheumatic Diseases 71, Suppl 3 (June 2013): 558.3–559. http://dx.doi.org/10.1136/annrheumdis-2012-eular.3204.
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Shin, K., S. H. Park, W. Park, H. J. Baek, Y. J. Lee, S. W. Kang, J. Y. Choe, et al. "SAT0286 Monthly Ibandronate Reduces Bone Loss in Osteopenic Women with Rheumatoid Arthritis Receiving Long-Term Glucocorticoids: A 48-Week Double-Blinded Randomized Placebo-Controlled Investigator-Initiated Trial." Annals of the Rheumatic Diseases 74, Suppl 2 (June 2015): 762.1–762. http://dx.doi.org/10.1136/annrheumdis-2015-eular.3204.
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Nozawa, Naoki, Yasushi Kawaguchi, Michiko Tanaka, Akihisa Kato, Ai Kato, Hiroshi Kimura, and Yukihiro Nishiyama. "Herpes Simplex Virus Type 1 UL51 Protein Is Involved in Maturation and Egress of Virus Particles." Journal of Virology 79, no. 11 (June 1, 2005): 6947–56. http://dx.doi.org/10.1128/jvi.79.11.6947-6956.2005.
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ABSTRACT The UL51 gene of herpes simplex virus type 1 (HSV-1) encodes a phosphoprotein whose homologs are conserved throughout the herpes virus family. Recently, we reported that UL51 protein colocalizes with Golgi marker proteins in transfected cells and that targeting of UL51 protein to the Golgi apparatus depends on palmitoylation of its N-terminal cysteine at position 9 (N. Nozawa, T. Daikoku, T. Koshizuka, Y. Yamauchi, T. Yoshikawa, and Y. Nishiyama, J. Virol. 77:3204-3216, 2003). However, its role in the HSV replication cycle was unknown. Here, we generated UL51-null mutants (FDL51) in HSV-1 to uncover the function of UL51 protein. We show that the mutant plaques were much smaller in size and that maximal titers were reduced nearly 100-fold compared to wild-type virus. Electron microscopy indicated that the formation of nucleocapsids was not affected by the deletion of UL51 but that viral egress from the perinuclear space was severely compromised. In FDL51-infected cells, a large number of enveloped nucleocapsids were observed in the perinuclear space, but enveloped mature virions in the cytoplasm, as well as extracellular mature virions, were rarely detected. These defects were fully rescued by reinsertion of the UL51 gene. These results indicate that UL51 protein is involved in the maturation and egress of HSV-1 virus particles downstream of the initial envelopment step.
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Peng, Xiao-Xiao, Ruoying Yu, Xue Wu, Shu-Yu Wu, Can Pi, Zhi-Hong Chen, Xu-Chao Zhang, et al. "Correlation of plasma exosomal microRNAs with the efficacy of immunotherapy inEGFR/ALKwild-type advanced non-small cell lung cancer." Journal for ImmunoTherapy of Cancer 8, no. 1 (January 2020): e000376. http://dx.doi.org/10.1136/jitc-2019-000376.
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BackgroundImmunotherapy has become an important treatment option for patients with advanced non-small cell lung cancer (NSCLC). At present, none of these existing biomarkers can effectively stratify true responders and there is an urgent need for identifying novel biomarkers. Exosomes derived from the serum of patients with cancer have been proven to be reliable markers for cancer diagnosis. Here, we explored the possibility of using plasma-derived exosomal microRNAs as potential biomarkers for optimal selection of patients with advancedEGFR/ALKnegative NSCLC to immunotherapy.MethodsFrom June 2017 to February 2019, 30 patients with advancedEGFR/ALKwild-type (WT) NSCLC who received PD-1/PD-L1 inhibitors were enrolled. The efficacy evaluation was conducted after every three cycles of treatment according to RECIST 1.1. Plasma samples of these patients were collected before the administration of PD-1/PD-L1 inhibitors as baseline, and after every three cycles if the patients achieved partial response (PR) or complete response. Plasma from seven healthy individuals was also collected as normal control. Exosomes were prepared by ultracentrifugation followed by total RNA extraction, and exosome-derived miRNAs were profiled using small RNA next-generation sequencing followed by differential expression analysis.ResultsIn order to identify biomarker for better response, all five patients who achieved PR and four patients with progressive disease (PD) at efficacy evaluation were included for differential expression analysis. Based on unsupervised hierarchical clustering, exosomal miRNA expression profile was significantly altered in patients with NSCLC compared with normal controls with a total of 155 differentially expressed exosomal miRNAs. Interestingly, hsa-miR-320d, hsa-miR-320c, and hsa-miR-320b were identified significantly upregulated in the PD groups compared with the PR group at baseline before the treatment. In addition, we identified that hsa-miR-125b-5p, a T-cell suppressor, showed a trend of increased expression in the PD group at baseline and was significantly downregulated in the post-treatment plasma exosomes compared with pre-treatment samples of the PR patients.ConclusionPatients with NSCLC represent unique plasma exosomal miRNA profiles. Hsa-miR-320d, hsa-miR-320c, and hsa-miR-320b were identified as potential biomarkers for predicting the efficacy of immunotherapy in advanced NSCLCs. When T-cell suppressor hsa-miR-125b-5p was downregulated during the treatment, the patients may obtain increased T-cell function and respond well to immunotherapy.
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Saadi, Soheyla, and Jeffrey L. Platt. "IMMUNOLOGY OF XENOTRANSPLANTATION." Life Sciences 62, no. 5 (December 1997): 365–87. http://dx.doi.org/10.1016/s0024-3205(97)00964-8.
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Konno, Yuki, Tsutomu Toki, Satoru Tandai, Gang Xu, Kiminori Terui, Shouichi Ohga, Seiji Kojima, et al. "Mutations in Ribosomal Protein Genes of Diamond-Blackfan Anemia Patients in Japan." Blood 114, no. 22 (November 20, 2009): 3204. http://dx.doi.org/10.1182/blood.v114.22.3204.3204.
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Abstract Abstract 3204 Poster Board III-141 Diamond-Blackfan anemia (DBA) is an inherited congenital bone marrow failure syndrome, characterized by red blood cell aplasia, macrocytic anemia, and increased risk of malignancy. Although anemia is the most prominent feature of DBA, the disease is also characterized by growth retardation and congenital malformations, which occur in about 40% of patients. Approximately 90% of patients present during the first year of life or in early childhood. Recent studies have shown that the disease is associated with heterozygous mutations in the ribosomal protein (RP) genes RPS19, RPS24, and RPS17, encoding small ribosomal subunit proteins, and in RPL5, RPL11 and RPL35a, encoding large ribosomal subunit proteins, in about 50% of patients with DBA in Western countries. There have been no studies to determine the incidence of these mutations in Asian patients with DBA. In this study, 44 probands (46 patients) with DBA in Japan were screened for mutations of the 6 known DBA genes RPS19, RPS24, RPS17, RPL5, RPL11, and RPL35a, in addition to RPS14, which is implicated in the 5q- syndrome, a subtype of myelodysplastic syndrome characterized by a defect in erythroid differentiation. Mutations in RPS19, which have been found in 25% of patients in Western countries, were detected in 6 probands (13.6%). Missense mutations were noted in 5 of these probands, and a frameshift mutation caused by a single-nucleotide insertion was found in 1 case. Three of 7 patients had multiple malformations. Novel mutations in RPL5 were identified in 3 probands (6.8%). Insertion of 2 nucleotides was found in 1 case, affecting the reading frame. Two cases had point mutations, which resulted in a loss of the first initiation codon. All 3 patients with RPL5 mutations had multiple physical anomalies. Remarkably, 2 of 3 patients with RPL5 mutations had cleft palate, whereas no other DBA patients presented with cleft palate. Mutations in RPL11 were identified in 2 patients (4.5%). Deletion of 1 or 2 nucleotides was found in each case, leading to a shift in the reading frame. In contrast to previous reports on patients with RPL11 mutations, thumb anomalies were not seen. Deletion of 1 nucleotide in RPS17 was identified in 1 patient (2.3%), resulting in introduction of a premature stop codon. RPS17 mutations are rare and have been only reported in 2 patients with DBA. Anomalies were not seen in our patient. In summary, RP gene mutations were identified in 27.3% of DBA index cases in Japan. No mutations were detected in RPS14, RPS24 and RPL35a. In Japan, the frequency of mutations in the RP genes appears to be lower than in Western countries. Mutations in RPL5 are associated with multiple physical abnormalities, including cleft palate. Disclosures No relevant conflicts of interest to declare.
Dissertations / Theses on the topic "3204 Immunology"
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Vijay, Rahul. "Prostaglandin regulation of immune responses against coronavirus infections." Diss., University of Iowa, 2016. https://ir.uiowa.edu/etd/3209.
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Prostaglandins (PG) are ubiquitous lipid mediators that play key roles in pathophysiological responses to infections. They are considered to have both pro and anti-inflammatory roles depending upon the time of inflammation, the receptors that they bind to and the tissues that they act upon. Hence given their pleiotropic effects, a perfect balance between the pro and anti-inflammatory functions of PGs are required to ensure that a controlled timely immune response is elicited to mediate protection and to avoid immunopathology.
PGD2 is one such PG that was reported to increase with age in the lungs of mice and to mediate an anti-inflammatory effect thereby blunting the immune response following Severe Acute Respiratory Syndrome – Coronavirus (SARS-CoV). Increase in PGD2 with age incapacitates respiratory dendritic cells (rDC) to migrate from lungs to the draining lymph node following SARS-CoV infection due to down regulation of CCR7 (a receptor for chemokines CCL19/21). Migration of rDCs to draining lymph nodes requires high expression of CCR7 and it's binding to CCL19/21, a chemokine that mediates migration of dendritic cells along its gradient. Although increase in levels of PGD2 might prove beneficial in high inflammatory conditions, it should be noted that high levels of such a potent anti-inflammatory mediator during the initiation of an immune response could prove detrimental. In chapter II of this thesis I show that age-related increases in oxidative stress result in the upregulation of a single phospholipase (PLA2) group II D (G2D) (PLA2G2D) with anti-inflammatory roles. PLA2G2D functions by releasing Arachidonic acid (AA) from the lipid membrane, which will be further metabolized to other pro-resolving/ anti-inflammatory lipid mediators including PGD2. I show that inducing oxidative stress in young mice as well as in human peripheral blood macrophages, results in the upregulation of PLA2G2D (probably as a counter mechanism against oxidative stress). Also increase in the expression levels of this gene during the course of SARS-CoV infection results in the upregulation of PGD2, which is completely abrogated in Pla2g2d-/- mice. I also show Pla2g2d/- middle-aged mice have low levels of PGD2 and that they are capable of mounting a strong immune response and survive the otherwise lethal SARS-CoV infection.
PGD2 is also a major PG in the brain and its role has been investigated in many non-infectious setting such as stroke and Alzheimer' disease. The PGD2 binding to one of its receptors DP1 has been shown to have primarily a neuro-protective role. In chapter III, I show that PGD2/DP1 signaling has beneficial effects in the brain of mice infected with a neurotropic strain of murine hepatitis virus (MHV) (rj2.2). In agreement with the neuro-protective role of PGD2, at least 60% of DP1-/- mice succumb to a sublethal dose of rj2.2. rj2.2 infection in these mice is characterized by a delay in the induction of IFN I response and lower activation status of microglia and macrophages in the brain. I also show that abrogation of DP1 signaling results in global defects in the immune system response to infection. Notably, a genome wide expression analysis using microarray, shows that a gene, Pydc3 with putative inflammasome inhibiting function is upregulated in WT mice compared to DP1-/- mice in the CD11b population of cells which primarily comprises microglia and macrophages. In line with the predicted function of Pydc3, DP1-/- mice have higher frequency and number of IL-1β+ producing microglia in the brain. Studies are underway to determine the exact role of DP1 signaling in Pydc3 expression as well as the role of this gene in inflammasome function.
Overall these studies emphasize the immuno-modulatory roles of PGs in the context of a viral infection. Thus, altering the levels of these lipid mediators at appropriate times during the course of infection might prove useful as an effective therapeutic strategy to decide the fate of an infection.
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Marquis, Miriam. "Étude du rôle de la MAP Kinase non-conventionnelle ERK3 dans le développement thymique et l'activation des lymphocytes T." Thèse, 2009. http://hdl.handle.net/1866/3203.
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Les voies de signalisation des MAP kinases (MAPK) conventionnelles jouent des rôles essentiels pendant le développement des lymphocytes T (LT) ainsi que lors de leur activation suite à la reconnaissance antigénique. En raison de ses différences structurelles ainsi que de son mode de régulation, ERK3 fait partie des MAPK dites non-conventionnelles. Encore aujourd’hui, les événements menant à l’activation de ERK3, ses substrats ou partenaires ainsi que sa fonction physiologique demeurent peu caractérisés. Nous avons entrepris dans cette thèse d’étudier le rôle de ERK3 lors du développement et de l’activation des LT en utilisant un modèle de souris déficient pour l’expression de ERK3. Nous avons premièrement établi que ERK3 est exprimée chez les thymocytes. Ensuite, nous avons évalué le développement thymique chez la souris ERK3-déficiente et nous avons observé une diminution significative de la cellularité aux étapes DN1, DP et SP CD4+ du développement des LT. La création de chimères hématopoïétiques ERK3-déficientes nous a permis de démontrer que la diminution du nombre de cellules observée aux étapes DN1 et DP est autonome aux thymocytes alors que le phénotype observé à l’étape SP CD4+ est dépendant de l’abolition simultanée de ERK3 dans l’épithélium thymique et dans les thymocytes. Une étude plus approfondie de l’étape DP nous a permis de démontrer qu’en absence de ERK3, les cellules DP meurent plus abondamment et accumulent des cassures doubles brins (DSB) dans leur ADN. De plus, nous avons démontré que ces cassures dans l’ADN sont réalisées par les enzymes RAG et qu’en absence de ces dernières, la cellularité thymique est presque rétablie chez la souris ERK3-déficiente. Ces résultats suggèrent que ERK3 est impliquée dans un mécanisme essentiel à la régulation des DSB pendant le réarrangement V(D)J de la chaîne du récepteur des cellules T (RCT). Dans le deuxième article présenté dans cette thèse, nous avons montré que ERK3 est exprimé chez les LT périphériques, mais seulement suite à leur activation via le RCT. Une fois activés in vitro les LT ERK3-déficients présentent une diminution marquée de leur prolifération et dans la production de cytokines. De plus, les LT ERK3-déficients survivent de façon équivalente aux LT normaux, mais étonnamment, ils expriment des niveaux plus faibles de la molécule anti-apoptotique Bcl-2. Ces résultats suggèrent que la prolifération réduite des LT ERK3-déficients est la conséquence d’une altération majeure de leur activation.
Ainsi, nos résultats établissent que ERK3 est une MAPK qui joue des rôles essentiels et uniques dans le développement thymique et dans l’activation des lymphocytes T périphériques. Grâce à ces travaux, nous attribuons pour la toute première fois une fonction in vivo pour ERK3 au cours de deux différentes étapes de la vie d’un LT.Classical MAP kinases (MAPK) play essential roles during T cell development and activation. ERK3 is a member of the MAPK family for which no physiological function has been described yet. Also, ERK3 is an atypical MAPK since its structure and mode of regulation are different from the conventional MAPK. Even today, the events leading to ERK3 activation and its substrates or partners are still largely unknown. We have studied in this thesis the role of ERK3 during T cell development and activation by using a mouse model in which ERK3 is not expressed. First, we have established that ERK3 is expressed in thymocytes. Next, we have evaluated thymic development in ERK3-deficient mice and we have observed a significant decrease in cell number at DN1, DP and CD4SP stages of T cell development. ERK3-deficient hematopoietic chimeras revealed that the DN1 and DP phenotype are T-cell autonomous, while abrogation of CD4SP development requires ERK3-deficiency in both thymocytes and thymic epithelium. By investigating further the DP stage, we have shown that ERK3-deficient DP thymocytes are more prone to apoptosis and also accumulate DNA double-strand breaks (DSBs). Moreover, we have shown that the increase DSBs are the direct consequence of RAG activity and that abolition of RAG almost restored thymic cellularity in ERK3-deficient mice. These results suggest that ERK3 is involved in an essential mechanism of DBSs regulation during TCR recombination. In the second article presented in this thesis, we have shown that ERK3 is expressed in peripheral T cell, but only when their TCR is activated. Also, ERK3-deficient T cells presented a strong reduction in proliferation and cytokine secretion following in vitro stimulation. Moreover, activated T cells lacking ERK3 are not more prone to death and surprisingly, they are unable to up-regulate the expression of the anti-apoptotic molecule Bcl-2 following TCR stimulation. These results suggest that the reduced proliferation of ERK3-deficient T cells is a consequence of their defective activation. Collectively, our results unveil essential and unsuspected roles for ERK3 in T cell development and activation. With this study, we establish for the first time an in vivo function for the atypical MAPK ERK3 in two different stages during T cell life.
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Chase, Jérémie Eric. "The Impact of a Single Intermittent Pneumatic Compression Bout on Performance, Inflammatory Markers, and Myoglobin in Football Athletes." 2017. http://hdl.handle.net/1993/32045.
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Intermittent Pneumatic Compression (IPC) use as a tool for recovery after exercise has recently become widespread among athletes. While there is strong anecdotal support for IPC, little research has been done to show its effectiveness in recovery. Eight collegiate football athletes were recruited and subjected to IPC or control conditions in a randomized crossover manner during off-season training. Countermovement jump (CMJ) and 10m sprint were evaluated before training, at 3 and 24 hours following training. Self-reported soreness, blood markers of inflammation [interleukin-6, interleukin-10, and monocyte chemoattractant protein-1 (MCP-1)] and muscle damage (myoglobin) were measured before training, post-training, post-recovery and at 3 and 24 hours post-training. Significant time effects were observed in MCP-1 and myoglobin (p < 0.05) indicating an inflammatory response and muscle damage. No group differences (p > 0.05) were observed between recovery interventions for all measures, suggesting that the IPC protocol used was not effective in this population.February 2017
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Beauchemin, Karine. "Dissection moléculaire de l’interaction de la DNA topoisomérase I avec la matrice extracellulaire et les fibroblastes." Thèse, 2009. http://hdl.handle.net/1866/3202.
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La sclérose systémique est une maladie autoimmune dont l’une des complications majeures est la fibrose. La DNA topoisomérase I (topo) est l’un des principaux autoantigènes associés à cette maladie. Toutefois, aucun lien n’a encore pu être établi entre la présence des anti-topo et le développement de la fibrose.
Les travaux antérieurs du laboratoire d’accueil ont montré une interaction directe de la topo avec la surface des fibroblastes et la matrice extracellulaire. Nous avons voulu caractériser ces interactions du point de vue moléculaire. La topo a donc été exprimée sous forme de 5 fragments, déterminés à partir de ses principaux domaines structuraux et de ses épitopes majeurs, chez E. coli. Les fragments purifiés ont été analysés pour leur interaction avec l’héparine, représentant les héparane sulfates de la surface des fibroblastes, et avec des protéines purifiées de la matrice extracellulaire.
Nous avons montré que le fragment topo-N est le principal responsable de l’interaction avec l’héparine, ce qui suggère donc l’implication potentielle de ce domaine dans l’interaction de la topo avec la surface des fibroblastes. Le fragment topo-DIDII est responsable de l’interaction avec la plupart des protéines de la matrice extracellulaire étudiées, alors que le fragment topo-H15 n’interagit qu’avec la vitronectine. Aucune interaction des fragments topo-DIII et topo-C n’a été décelée.
Ces résultats pourront maintenant servir à mieux comprendre le rôle potentiel de la topo et des autoanticorps circulants anti-topo dans la fibrose présente chez les personnes atteintes de sclérose systémique en contribuant à l’identification de la cible de la topo sur les fibroblastes.Systemic sclerosis is an autoimmune disease in which one of the major complications is fibrosis. DNA topoisomerase I (topo) is a major autoantigen associated with this disease. However, no link has yet been established between the presence of anti-topo and the development of fibrosis. Previous work of the host laboratory showed a direct interaction of the topo with the surface of fibroblasts and extracellular matrix. We wanted to characterize these interactions at the molecular level. Topo was expressed in 5 fragments, determined from its main structural domains and its major epitopes, in E. coli. The purified fragments were analyzed for their interaction with heparin, representing heparan sulfates on the surface of fibroblasts, and with purified proteins of the extracellular matrix. We have shown that the topo-N fragment is responsible for interaction with heparin, suggesting hence, potential involvement of this domain in the interaction of topo with the surface of fibroblasts. The topo-DIDII fragment is responsible for the interaction with most proteins of the extracellular matrix studied, whereas the topo-H15 fragment only binds to vitronectin. No interaction of fragments topo-DIII and topo-C was found. These results can now be used to better understand the potential role of topo and circulating anti-topo autoantibodies in the fibrosis present in patients with systemic sclerosis in helping to identify the target of topo on fibroblasts.
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Pudkasam, Supa. "Physical activity motivation and self-directed physical activity in female breast cancer survivors." Thesis, 2021. https://vuir.vu.edu.au/42516/.
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Mikkelsen, Kathleen. "The Effects of Vitamin B6 and B12 on Inflammation and Cancer." Thesis, 2022. https://vuir.vu.edu.au/43344/.
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We are only just beginning to understand the intricate relationship between nutrition, immune health, inflammation, and cancer. Epidemiological studies have demonstrated a clear association between inflammation and cancer development. Both undernutrition and overnutrition (malnutrition) have been shown to have a significant impact on immune health and function. Even in countries where food is plentiful, a diet high in processed food can be high in calories whilst being nutritionally deficient. The emergence of B vitamins as anti-inflammatory and anti-cancer agents is an area which in recent years has gained interest within the scientific community and as the development of genetic and epigenetic investigative techniques becomes more available to a greater number of researchers, there is ongoing investigation occurring concerning how nutrition affects gene expression. Low blood serum vitamin B6 is frequently noted in patients with high inflammatory markers and vitamin B6 supplementation has previously been shown to downregulate inflammation and oxidative stress in both inflammation and as an anti-cancer mechanism. In contrast, the effects of vitamin B12 supplementation have been shown within the literature to be ambiguous with links both to cancer progression and pro-inflammatory actions versus tumour regression and anti-inflammatory properties. The purpose of this thesis was to ascertain, with greater clarity, the mechanisms of action of high dose vitamin B6 and B12 on inflammation and cancer. This was achieved by conducting studies on both cancer and immune cells and using protein and gene studies to ascertain the effects of high-dose vitamin B supplementation. It was found that high dose vitamin B6 was shown to have an anti-proliferative effect on promonocytic lymphoma cells, likely due to a downregulation of the mevalonate pathway (MVP) whereby vitamin B6 acted in a ‘steroid-like' fashion to reduce MVP, restoring mutant p53 function and re-establishing the G1/S checkpoint. Vitamin B6
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was also shown to have a broad-spectrum, anti-inflammatory effect on key inflammatory pathways in lipopolysaccharide (LPS) stimulated monocytes. In contrast, vitamin B12 supplementation produced an upregulation in key inflammatory gene expressions and showed a dose-dependent effect on inflammation. The important and novel findings from this thesis conclude, that high dose vitamin B6 may prove to be an important nutraceutical agent in both inflammatory and oncological medicine and that B12 over-supplementation may potentially contribute to inflammation and tumourigenesis so caution should be taken when supplementing in dosages above the recommended daily intake.
Books on the topic "3204 Immunology"
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Humanized Mice (Current Topics in Microbiology and Immunology Book 324). Springer, 2008.
Find full textBook chapters on the topic "3204 Immunology"
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Ackers, J. P. "Immunologic Aspects of Human Trichomoniasis." In Trichomonads Parasitic in Humans, 36–52. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3224-7_4.
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Kaufmann, Stefan H. E., and Dieter KabelitZ. "Preface to the second edition." In Immunology of Infection, xvii. Elsevier, 2002. http://dx.doi.org/10.1016/s0580-9517(02)32084-1.
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Czuprynski, Charles J., and James F. Brown. "Isolation and preparation of lymphocytes from infected animals for in vitro analysis." In Immunology of Infection, 233–47. Elsevier, 2002. http://dx.doi.org/10.1016/s0580-9517(02)32094-4.
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Corr, Maripat, Delphine J. Lee, and Eyal Raz. "DNA vaccines: Fundamentals and practice." In Immunology of Infection, 527–50. Elsevier, 2002. http://dx.doi.org/10.1016/s0580-9517(02)32104-4.
Full textConference papers on the topic "3204 Immunology"
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Liu, Pu, Jade Jaffar, Elizabeth Swisher, Karl Erik Hellstrom, and Ingegerd Hellström. "Abstract LB-320: Inhibition of TGFß1 improves the therapeutic efficacy of non-immunologic tumor cell based vaccine." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-320.
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