Dissertations / Theses on the topic 'Periodontal disease Molecular aspects'
To see the other types of publications on this topic, follow the link: Periodontal disease Molecular aspects.
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 dissertations / theses for your research on the topic 'Periodontal disease Molecular aspects.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse dissertations / theses on a wide variety of disciplines and organise your bibliography correctly.
1
Gully, Neville. "Studies on the growth and metabolism of Eikenella corrodens /." Title page, summary and table of contents only, 2000. http://web4.library.adelaide.edu.au/theses/09PH/09phg973.pdf.
2
Irani, Dilshad Minocher. "Role of the surface associated material of Eikenella corrodens in bone resorption associated with periodontal disease : a research thesis submitted in fulfilment of the requirements for the degree of Master of Science in Dentistry." Title page, contents and summary only, 1998. http://web4.library.adelaide.edu.au/theses/09DSM/09dsmi65.pdf.
3
Mooney, John. "Molecular and cellular aspects of the humoral immune response in periodontal disease and other related conditions." Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321510.
4
Kennedy, Rebekah Storm. "Microbiological and immunological aspects of equine periodontal disease." Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/8064/.
Abstract:
Periodontal disease is a common and painful condition in the horse. Although awareness of the condition is growing amongst the veterinary profession and horse owners, the presence of the disease is often overlooked and treatment can be difficult. Despite this, there have been few recent studies of the aetiopathogenesis of the condition. Certain species of bacteria may act as periodontal pathogens, stimulating a destructive inflammatory response in periodontal tissues and this has been well recognised as being important to the aetiopathogenesis of the disease in man. However few equine studies on this aspect of the disease have been carried out. The main aims of this study were: - 1) to identify the bacteria associated with a healthy oral cavity and periodontitis in horses using culture dependent and independent methods; 2) to assess the differences in bacterial populations between the healthy and periodontitis groups and identify putative pathogens; 3) to quantify the expression patterns of TLRs 2, 4 and 9, the pro-inflammatory cytokines IL-1β and TNFα, anti-inflammatory cytokine IL-10 and Th1/Th2/Th17 cytokines IL-4, IL-6/ IL-12, IFNɣ/ IL-17, within gingival tissue from each sample group; 4) to use matched data to establish if associations exist between the presence and quantity of bacterial species present and TLR expression and 5) to determine activation of TLRs 2, 4 and 9 by putative pathogens using specific in- vitro TLR assays. Swabs were taken from the gingival sulcus of 42 orally healthy horses and plaque samples were taken from the periodontal pockets of 61 horses with periodontal disease. The location and grade of the lesion was noted and an equine dental chart completed for each case. Bacteria were identified using high throughput 16S rRNA gene sequencing, QPCR, whole genome sequencing and conventional culture followed by 16S gene sequencing. Gingival biopsies were taken from 13 orally healthy horses and 20 horses with periodontitis and gene expression of TLR 2, TLR 4, TLR 9, IL-1β, IL-4, IL-6, IL-10, IL-12, IL-17, TNFα and IFNɣ was measured. THP-1X Blue, MyD88 THP-1X Blue, HEK hTLR 2 Blue and HEK hTLR 4 Blue human cell lines were co-cultured with putative periodontal pathogens and their response measured via level of secreted embryonic alkaline phosphatase. Clinical, microbiological and immunological data underwent cross-matching analysis. Microbial populations showed 89% dissimilarly between oral health and periodontitis with a less diverse population present in diseased equine periodontal pockets. The most discriminative bacteria between health and disease identified at genus level were Fusobacteria and Acinetobacter in health and Pseudomonas and Prevotella in periodontitis. The most abundant genera were Gemella (36.5%), Pseudomonas (14%) and Acinetobacter (8%) in orally healthy samples and Pseudomonas (25%), Prevotella (14%) and Acinetobacter (9.4%) in periodontitis samples. Whole genome sequencing revealed the presence of 75 species of Prevotella in the equine oral cavity and a significantly higher number of reads corresponding to Prevotella bivia, Prevotella dentalis, Prevotella denticola, Prevotella intermedia, Prevotella melaninogenica, Prevotella nigrescens were noted in diseased samples. Significant increases in expression of TLR 4 mRNA, TLR 9 mRNA and, in particular TLR 2, mRNA were noted in diseased equine gingival tissue in addition to increased pro-inflammatory and anti-inflammatory cytokine mRNA expression. Presence of P. intermedia was significantly positively correlated with expression of TLR 2 in equine periodontitis. In addition, the presence of Aggregatibacter actinomycetemcomitans was positively associated with disease severity and expression of TLR 4 mRNA in the horse. Co-culture of periodontal pathogens with human cell lines revealed that the innate immune response to the presence of these bacteria is mainly mediated through TLR 2 activation. The use of both culture dependent and culture independent methods to investigate the equine oral microbiome has provided significant breadth and depth of information on the microbiology of equine periodontal disease. Microbial populations are significantly different as expected and bacteria belonging to the Prevotella genus have been strongly implicated in the aetiopathogenesis of the condition. The innate immune response produced in periodontally diseased equine gingival tissue has been characterised for the first time in the horse.
5
Ng, Kwai-sang Sam, and 吳桂生. "Psychological perspectives of periodontal disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B36918210.
6
Preber, Hans. "Cigarette smoking and periodontal disease clinical and therapeutic aspects /." Stockholm : Dept. of Periodontology, Karolinska Institutet, 1986. http://books.google.com/books?id=4ulpAAAAMAAJ.
7
Porter, S. R. "Immunological aspects of rapidly progressive periodontitis." Thesis, University of Bristol, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377350.
8
Sörgjerd, Karin. "Molecular Aspects of Transthyretin Amyloid Disease." Doctoral thesis, Linköpings universitet, Biokemi, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-12566.
Abstract:
This thesis was made to get a deeper understanding of how chaperones interact with unstable, aggregation prone, misfolded proteins involved in human disease. Over the last two decades, there has been much focus on misfolding diseases within the fields of biochemistry and molecular biotechnology research. It has become obvious that proteins that misfold (as a consequence of a mutation or outer factors), are the cause of many diseases. Molecular chaperones are proteins that have been defined as agents that help other proteins to fold correctly and to prevent aggregation. Their role in the misfolding disease process has been the subject for this thesis. Transthyretin (TTR) is a protein found in human plasma and in cerebrospinal fluid. It works as a transport protein, transporting thyroxin and holo-retinol binding protein. The structure of TTR consists of four identical subunits connected through hydrogen bonds and hydrophobic interactions. Over 100 point mutations in the TTR gene are associated with amyloidosis often involving peripheral neurodegeneration (familial amyloidotic polyneuropathy (FAP)). Amyloidosis represents a group of diseases leading to extra cellular deposition of fibrillar protein known as amyloid. We used human SH-SY5Y neuroblastoma cells as a model for neurodegeneration. Various conformers of TTR were incubated with the cells for different amounts of time. The experiments showed that early prefibrillar oligomers of TTR induced apoptosis when neuroblastoma cells were exposed to these species whereas mature fibrils were not cytotoxic. We also found increased expression of the molecular chaperone BiP in cells challenged with TTR oligomers. Point mutations destabilize TTR and result in monomers that are unstable and prone to aggregate. TTR D18G is naturally occurring and the most destabilized TTR mutant found to date. It leads to central nervous system (CNS) amyloidosis. The CNS phenotype is rare for TTR amyloid disease. Most proteins associated with amyloid disease are secreted proteins and secreted proteins must pass the quality control check within the endoplasmic reticulum (ER). BiP is a Hsp70 molecular chaperone situated in the ER. BiP is one of the most important components of the quality control system in the cell. We have used TTR D18G as a model for understanding how an extremely aggregation prone protein is handled by BiP. We have shown that BiP can selectively capture TTR D18G during co-expression in both E. coli and during over expression in human 293T cells and collects the mutant in oligomeric states. We have also shown that degradation of TTR D18G in human 293T cells occurs slower in presence of BiP, that BiP is present in amyloid deposition in human brain and mitigates cytotoxicity of TTR D18G oligomers.Denna avhandling handlar om proteiner. Särskilt de som inte fungerar som de ska utan har blivit vad man kallar ”felveckade”. Anledningen till att proteiner veckas fel beror ofta (men inte alltid) på mutationer i arvsmassan. Felveckade proteiner kan leda till sjukdomar hos människor och djur (man brukar tala om amyloidsjukdomar), ofta av neurologisk karaktär. Exempel på amyloidsjukdomar är polyneuropati, där perifera nervsystemet är drabbat, vilket leder till begränsad rörelseförmåga och senare till förlamning; och Alzheimer´s sjukdom, där centrala nervsystemet är drabbat och leder till begränsad tankeförmåga och minnesförluster. Studierna som presenteras i denna avhandling har gått ut på att få en bättre förståelse för hur felveckade proteiner interagerar med det som vi har naturligt i cellerna och som fungerar som skyddande, hjälpande proteiner, så kallade chaperoner. Transtyretin (TTR) är ett protein som cirkulerar i blodet och transporterar tyroxin (som är ett hormon som bland annat har betydelse för ämnesomsättningen) samt retinol-bindande protein (vitamin A). I TTR genen har man funnit över 100 punktmutationer, vilka har kopplats samman med amyloidsjukdomar, bland annat ”Skellefteåsjukan”. Mutationer i TTR genen leder ofta till att proteinet blir instabilt vilket leder till upplösning av TTR tetrameren till monomerer. Dessa monomerer kan därefter sammanfogas på nytt men denna gång på ett sätt som är farligt för organismen. I denna avhandling har fokus legat på en mutation som kallas TTR D18G, vilken har identifierats i olika delar av världen och leder till en dödlig form av amyloidos i centrala nervsystemet. Det chaperon som vi har studerat benämns BiP och är beläget i en cellkomponent som kallas för det endoplasmatiska retiklet (ER). I ER finns cellens kontrollsystem i vilket det ses till att felveckade proteiner inte släpps ut utan istället bryts ned. Denna avhandling har visat att BiP kan fånga upp TTR D18G inuti celler och där samla mutanten i lösliga partiklar som i detta fall är ofarliga för cellen. Avhandligen har också visat att nedbrytningen av TTR D18G sker mycket långsammare när BiP finns i riklig mängd.
9
Boström, Lennart. "Tobacco smoking and periodontal disease : some clinical, microbiological and immunological aspects /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4456-3/.
10
Hanley, Shirley Anne. "Molecular characterisation of an immunodominant 55kDa surface antigen of Porphyromonas gingivalis W50." Thesis, Queen Mary, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312824.
11
Watkins, Craig Allen. "Molecular aspects of punta toro virus." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239272.
12
Jim, Jin-to, and 詹展韜. "Genetics and molecular characterization of degenerative disc disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B35720189.
13
Ye, Ping. "Autoimmunity in chronic periodontitis." University of Sydney, 2003. http://hdl.handle.net/2123/4256.
Abstract:
Doctor of PhilosophyProfound perturbation of epithelial structure is a characteristic feature of the immunopatholoical response to bacterial antigens considered to be central in the pathogenesis of the destructive lesion of periodontitis. The pathological basis for the disturbance of epithelial structure is not understood. It was demonstrated that the structural integrity and functional differentiation of the lining epithelium is compromised in relation to inflammatory changes associated with destructive periodontitis. In the pathological lining epithelium of the periodontal pocket there was a marked reduction of epithelial cadherin important in intercellular adhesion, of involucrin, a marker of terminal differentiation, and of the gap junction connexions that form intercellular communication channels. These changes were associated with alterations of filamentous actin expression, collectively indicating profound perturbation of epithelial structure. The data reported support the concept that the ability of the pathological lining epithelium to function as an effective barrier against the ingress of microbial products into the tissues is severely compromised (Ye et al., 2000). In addition, a recent study (Ye et al., 2003) by Western analysis of serum IgG from all 22 patients with chronic periodontitis tested indicated recognition of multiple epithelial components in individual patterns. In contrast, subjects with a healthy periodontium displayed only trace recognition of epithelial antigens. Levels of epithelial-reactive antibodies were significantly correlated with attachment loss as an indication of disease activity. To investigate a possible relationship between the bacterial flora adjacent to the diseased sites and the presence of epithelial-reactive antibodies, subgingival plague samples were taken from deep periodontal pockets and cultured anaerobically. Gram positive bacteria containing antigens potentially cross-reactive with epithelial cells were reproducibly isolated by probing membrane colony lifts with affinity-isolated (epitheial-specific) antibodies. The bacteria were identified as streptococci (S. mitis, S. constellatus and two S. intermedius strains) and Actinomyces (A. georgiae, and A. sp. oral clone) by 16S rDNA sequence homology. Recognition by affinity-isolated antibodies of antigens from the captured organisms was confirmed by Western analysis. Conversely, absorption of affinity-isolated antibodies with bacterial species specifically reduced subsequent recognition of epithelial antigens. To identify the auto-antigens, a human keratinocyte cDNA expression library in Lambda phage was probed using a pooled sera. Groups of responders were detected for CD24 (a recently described adhesion molecule also known as P-selectin ligand), antioxidant protein 2 (a newly recognised member of the thiol-dependment anti-oxidant proteins), lavtate dehydrogenase A, the transcription factor NFAT5, and for three genes encoding novel proteins. Six identified bacteria, especially S intermedius were demonstrated to absorb antibodies reaching with identified auto-antigens in patterns varying between individuals. This evidence indicated that during the course of periodontits, subjects develop increased levels of antibodies to common oral bacteria amongst which are included tissue cross-reactive antigens. Periodontitis could therefore present a risk for the subsequent initiation or exacerbation of a broad spectrum of disease processes including autoimmune, inflammatory, proliferative and degenerative disorders.
14
BrÃgido, Jandenilson Alves. "Prevalence and distribution of Aggregatibacter actinomycetemcomitans serotypes in periodontal disease Brazilian subjects." Universidade Federal do CearÃ, 2012. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=9056.
Abstract:
nÃo hÃStudies suggest that subjects with severe periodontal lesions are more likely to colonize Aggregatibacter actinomycetemcomitans. This species is genetically heterogeneous and can be grouped into six serotypes (a-f), which may differ regarding virulence characteristics. Ethnic differences and geographic population can influence the distribution and prevalence of these serotypes regarding periodontal disease. The aims of this dissertation, comprised of two manuscripts, were to review the literature concerning A. actinomycetemcomitans serotypes regarding to periodontal status and geographic origin of individuals (chapter 1); and to investigate the prevalence and distribution of A. actinomycetemcomitans serotypes in Brazilian subjects with chronic and aggressive periodontitis, identifying possible relationship of the different A. actinomycetemcomitans serotypes with periodontal disease (chapter 2). In study 1 was performed a systematic review of the pertinent literature related to the issue and in study 2, subgingival plaque sample of 71 subjects with aggressive or chronic periodontitis positive to A. actinomycetemcomitans were analysed by polymerase chain reaction (PCR). The literature analysis presented in study 1 showed that different ethnic groups are preferentially colonized by different A. actinomycetemcomitans serotypes. Serotypes a, b and c were largely found, and serotype c was the most prevalent in the majority of studies. The results of study 2 demonstrated that serotype c was detected with the highest frequency and serotypes d-f were not detected. It was also observed that individuals with aggressive periodontitis showed higher prevalence of both serotypes b and c (p<0.05), and in chronic periodontitis subjects the serotype c was significantly more prevalent (p<0.05). In conclusion, the results of these studies suggest that the relationship between the different serotypes and periodontal conditions remains unclear (chapter 1). Serotype c was dominant among Brazilian subjects with periodontal disease and aggressive periodontitis subjects were associated both serotypes b and c (chapter 2).
Estudos indicam que indivÃduos com lesÃes periodontais mais severas apresentam maior probabilidade de serem colonizados por Aggregatibacter actinomycetemcomitans. Essa espÃcie à geneticamente heterogÃnea e pode ser agrupada em seis sorotipos (a-f), que podem diferir quanto a suas caracterÃsticas de virulÃncia. As diferenÃas Ãtnicas e populaÃÃes geogrÃficas podem influenciar na distribuiÃÃo e prevalÃncia desses sorotipos em relaÃÃo ao tipo de doenÃa periodontal. Os objetivos dessa dissertaÃÃo, constituÃda por dois artigos, foram: revisar a literatura concernente aos sorotipos de A. actinomycetemcomitans em relaÃÃo à condiÃÃo periodontal e origem geogrÃfica dos indivÃduos (capÃtulo 1); e avaliar a prevalÃncia e distribuiÃÃo dos sorotipos de A. actinomycetemcomitans em pacientes brasileiros com periodontite crÃnica e agressiva, identificando a possÃvel relaÃÃo dos diferentes sorotipos de A. actinomycetemcomitans com a patologia periodontal (capÃtulo 2). No estudo 1, foi realizada uma revisÃo sistemÃtica da literatura pertinente ao assunto e no estudo 2, amostras de biofilme bacteriano subgengival de 71 pacientes com periodontite agressiva ou crÃnica positivos para A. actinomycetemcomitans foram analisadas atravÃs da reaÃÃo em cadeia da polimerase (PCR). A anÃlise da literatura apresentada no estudo 1 mostrou que diferentes grupos Ãtnicos sÃo preferencialmente colonizados por diferentes sorotipos de A. actinomycetemcomitans. Os sorotipos a, b e c foram largamente encontrados e o sorotipo c foi o mais prevalente na maioria dos estudos. Os resultados do estudo 2 demonstraram que o sorotipo c foi encontrado com maior frequÃncia e os sorotipos d-f nÃo foram detectados. Foi verificado tambÃm que indivÃduos com periodontite agressiva apresentaram maior prevalÃncia de ambos os sorotipos b e c (p<0.05), e que em pacientes com periodontite crÃnica o sorotipo c foi significativamente mais prevalente (p<0.05). Em conclusÃo, os resultados desses estudos indicam que a relaÃÃo entre os diferentes sorotipos e a condiÃÃo periodontal permanece obscura (capÃtulo 1). O sorotipo c foi dominante entre pacientes brasileiros com doenÃa periodontal e os indivÃduos com periodontite agressiva foram associados com os sorotipos b e c (capÃtulo 2).
15
Chen, Zheng-Yi. "Molecular biology of X-chromosome disease." Thesis, University of Oxford, 1992. http://ora.ox.ac.uk/objects/uuid:8214a2f6-0bfa-4ea4-8f48-b8a20f29318c.
Abstract:
Genomic clones were isolated and characterized using the human monoamine oxidase A (MAOA) cDNA to screen a phage library, constructed from a human 4X cell line (48, XXXX). The genomic contig derived from overlapping phage clones showed that the size of the MAOA gene is over 80 kb. Exon-containing fragments from these phage clones were subcloned and sequenced. The data from this showed that the MAOA gene consists of 15 exons. A YAC (yeast artificial chromosome) isolated using the MAOA cDNA was characterized. This YAC was found to contain both the MAOA and the MAOB genes. Using PFGE (pulsed-field gel electrophoresis) to investigate the YAC, it was found that the MAOA and the MAOB genes are located within 50 kb and adjacent to each other. The two genes are localized in a 3'-to-3' fashion, suggesting their expression may be regulated independently. The analysis of the homology shown by the two genes clearly demonstrated that they were derived from duplication of a common ancestral gene. A CpG island was discovered to be associated with the 5' end of both genes. A restriction map of -2.5 Mb of genomic DMA around the MAO genes was generated by PFGE. Long-range mapping defined the physical relationship between the marker L1.28 and the MAO genes as L1.28_MAOA_MAOB. A number of genetic diseases have been linked to the Xp11.3 region. Strong linkage was known to exist between the Norrie disease locus and L1.28. Studies showed that some of the Norrie patients have deletions encompassing the region which contains L1.28 as well as the MAO genes. Another YAC isolated by using L1.28 as the probe was also characterized. A phage library was constructed from the L1.28 YAC and the end clones were isolated. Studies on some of the Norrie deletion patients showed that the proximal end clone of the YAC was retained in one of the deletion patients. Previous studies had shown that the Norrie disease locus was also localized proximal to the 5' end of the MAOB gene. The combined information placed the disease locus to an interval of 240 kb within the YAC. More phage clones were characterized in order to define further the region for the Norrie locus which was finally localized within 160 kb. A YAC fragment of 160 kb was isolated and used to screen two human retinal cDNA libraries. Among the cDNAs isolated, one group was found to be deleted in some of the Norrie patients previously without any known deletion, which established their candidacy as the transcripts of the Norrie disease locus. Further characterization of the candidate gene showed that it is conserved across species. The expression of the gene was detected in various tissues. The homology shared between the NDP gene and some of the growth factor binding proteins suggests its role in neural cell proliferation and differentiation.
16
許育勳 and Yuk-fun Hui. "Molecular studies of X-linked chronic granulomatous disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1996. http://hub.hku.hk/bib/B31214150.
17
Hall, Richard James, and n/a. "Chromosome 18 and autoimmune disease." University of Otago. Department of Biochemistry, 2005. http://adt.otago.ac.nz./public/adt-NZDU20070221.141018.
Abstract:
The autoimmune diseases embody a diverse range of common human conditions that are caused by a loss of self-tolerance in the host immune system to a specific organ or tissue type. Approximately 5% of the general population are affected by autoimmune diseases which include type 1 diabetes (T1D), rheumatoid arthritis (RA) and Graves disease (GD). The majority of the autoimmune diseases are multifactorial in origin, brought about by a combination of both environmental and genetic factors. Numerous susceptibility loci have been identified for each autoimmune disease and a number of these loci have been shown to be shared amongst the autoimmune diseases. The fine-mapping of susceptibility loci to the underlying disease genes remains the current challenge facing complex disease genetics. This project aimed to further characterise the autoimmune disease susceptibility locus IDDM6 on chromosome 18q12-21. This was achieved by using a comparative mapping approach that incorporates the study of genetic association in human autoimmune disease alongside the consomic mapping of the orthologous region in the non-obese diabetic (NOD) mouse model of autoimmunity.
Deleted in colorectal carcinomas (DCC) provided a strong candidate gene at IDDM6 and the resident R201G polymorphism was identified as a functional candidate A potential mechanism for the R201G polymorphism involvement in T1D aetiology was identified where the polymorphism may affect the ability of DCC to induce apoptosis in vitro. However, no evidence for R201G association could be detected in autoimmune disease case-control datasets from the New Zealand (NZ) population (T1D n = 428, RA n = 730, autoimmune thyroid disease n = 192 (AITD); versus n = 1246 healthy controls). In addition, no evidence for R201G involvement in T1D could be provided in a transmission disequilibrium test (TDT) incorporating 382 affected sib-pair families (54.2% transmission; P = 0.15). Significant association of R201G with GD was detected in a United Kingdom (UK) dataset (P = 0.002) from the Newcastle population (423 cases vs. 393 controls) but this was not replicated in an additional dataset from the UK Birmingham population (731 cases vs 668 controls; P = 0.81). It was concluded that the R201G polymorphism may encode susceptibility to GD but is unlikely to be the sole aetiological variant that accounts for the linkage previously observed at IDDM6 in autoimmune disease. To further investigate DCC as a positional candidate at IDDM6, five SNPs were selected from a 100 kb window surrounding a DCC-resident microsatellite that had previously been associated with T1D, called "88,21". The five SNPs were genotyped in the NZ T1D dataset, and the ascertainment of estimated haplotypes in this dataset revealed association of a rare haplotype with T1D, called haplotype H (3.31% cases vs 1.17% controls; P = 0.0044), in addition to global association of all haplotypes (P = 0.018). Haplotype H was also associated in an independent case-control dataset from the UK comprised of 400 T1D subjects and 443 healthy controls (P = 0.038). Maximum support for association of haplotype H was extended when both the UK and NZ T1D datasets were combined (P = 0.0017). Association of haplotype H could not be verified in a family-based test for association using the 382 UK T1D families (P = 0.40). However, the inclusion of the DCC SNPs in a TDT analysis of the published DCC-resident microsatellites "88,21" and "55,26", that had been used to identify IDDM6, extends support for the previously-associated 2-10 haplotype (2-10 refers to the published allele nomenclature at "88,21" and "55,26" respectively; 2-10-haplotype A; 59.6% T; P = 0.0058). There was no evidence for association of the five SNPs with RA or AITD when using either individual SNP analyses or estimated haplotypes in the NZ datasets. A similar lack of association was reported for the UK Newcastle GD dataset. Taken together, these data further support DCC, or a nearby gene, as conferring susceptibility to T1D.
The human genetic data that supports IDDM6 involvement in autoimmune disease is further strengthened by consomic mapping of the orthologous region in mouse, using the non-obese diabetic mouse (NOD) model of autoimmune disease. In this thesis, the first evidence for a diabetes and thyroiditis susceptibility locus on mouse chromosome 18 is presented, which have been designated Idd21 and Sat1 respectively. This was achieved by using a chromosome-replacement strain with chromosome 18 derived from the diabetes-resistant Biozzi ABH strain on a diabetes-susceptible NOD genome, called NOD.ABH[Chr�⁸]. Mouse chromosome 18 contains orthology to both IDDM6 and the rat diabetes-susceptibility locus Iddm3. The NOD.ABH[Chr�⁸] mice showed a dramatic and significant reduction in diabetes incidence (30% of females were affected by 7 months of age versus 85% in NOD; P <0.0001) and that of thyroiditis (15.5% at 12 months compared to 37.4% in NOD; P <0.002).
The comparative mapping of the chromosome 18 autoimmune susceptibility locus IDDM6 in human and mouse presented in this thesis provides further support for this locus. This research also clearly defines the next steps required to fine-map IDDM6 to the underlying disease genes, especially in regard to the DCC gene.
18
Wescott, David Clark, and n/a. "Osteogenic gene expression by human periodontal ligament cells under cyclic mechanical tension." University of Otago. School of Dentistry, 2008. http://adt.otago.ac.nz./public/adt-NZDU20081202.131453.
Abstract:
Background and objectives: The most widely accepted tooth movement model is defined by the pressure-tension hypothesis. An orthodontic force applied to a tooth generates areas of compression and tension in the periodontal ligament (PDL), which are transmitted to the alveolar bone. Areas of tissue exposed to tensile strain undergo bone deposition, whereas areas of tissue exposed to compressive strain undergo bone resorption. We propose that human PDL cells in monolayer culture exposed to tensile mechanical strain would express multiple genes involved in osteogenesis.
Materials and Methods: Human PDL cells were isolated and cultured from premolar teeth that were extracted for orthodontic reasons. These cells were plated on control and experimental Uniflex[TM] plates. Using a Flexercell FX4000 strain unit, PDL cells on experimental plates were exposed to a 12% uni-axial cyclic strain for 6 seconds out of every 90 seconds over a 24 hour period. RNA was extracted from the PDL cells at 6 hours, 12 hours and 24 hours. The differential expression of 78 genes implicated in osteoblast differentiation and bone metabolism was analysed using real-time reverse transcriptase polymerase chain reaction (RT-PCR) array technology.
Results: Of the 78 genes tested, sixteen genes showed statistically significant (p<0.05) changes in expression in response to the mechanical strain regime. Eight genes were up-regulated (ALPL, BMP2, BMP6, COL2A1, ICAM1, PHEX, SOX9, and VEGFA) and eight genes were down-regulated (ANXA5, BMP4, COL11A1, COL3A1, EGF, ITGB1, MSX and SMAD1).
Conclusions: This study has demonstrated that cultured human PDL cells express multiple osteogenic genes under tensile strain, which suggests that PDL cells may have a potential role in osseous remodeling during tooth movement.
Key Words: Tooth movement, human PDL cells, tensile mechanical strain, osteogenic genes, real-time RT-PCR array, and Flexercell FX4000.
19
Ingelson, Martin. "Molecular aspects of tau proteins in Alzheimer's disease and frontotemporal dementia /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4904-2/.
20
Guidotti, Serena <1985>. "Molecular basis of Osteoarthritis and aspects of cellular senescence in disease." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2015. http://amsdottorato.unibo.it/6751/.
Abstract:
The aim of this study is to investigate on some molecular mechanisms contributing to the pathogenesis of osteoarthritis (OA) and in particular to the senescence of articular chondrocytes. It is focused on understanding molecular events downstream GSK3β inactivation or dependent on the activity of IKKα, a kinase that does not belong to the phenotype of healthy articular chondrocytes. Moreover, the potential of some nutraceuticals on scavenging ROS thus reducing oxidative stress, DNA damage, and chondrocyte senescence has been evaluated in vitro.
The in vitro LiCl-mediated GSK3β inactivation resulted in increased mitochondrial ROS production, that impacted on cellular proliferation, with S-phase transient arrest, increased SA-β gal and PAS staining, cell size and granularity. ROS are also responsible for the of increased expression of two major oxidative lesions, i.e. 1) double strand breaks, tagged by γH2AX, that associates with activation of GADD45β and p21, and 2) 8-oxo-dG adducts, that associate with increased IKKα and MMP-10 expression. The pattern observed in vitro was confirmed on cartilage from OA patients.
IKKa dramatically affects the intensity of the DNA damage response induced by oxidative stress (H2O2 exposure) in chondrocytes, as evidenced by silencing strategies. At early time point an higher percentage of γH2AX positive cells and more foci in IKKa-KD cells are observed, but IKKa KD cells proved to almost completely recover after 24 hours respect to their controls. Telomere attrition is also reduced in IKKaKD. Finally MSH6 and MLH1 genes are up-regulated in IKKαKD cells but not in control cells.
Hydroxytyrosol and Spermidine have a great ROS scavenging capacity in vitro. Both treatments revert the H2O2 dependent increase of cell death and γH2AX-foci formation and senescence, suggesting the ability of increasing cell homeostasis. These data indicate that nutraceuticals represent a great challenge in OA management, for both therapeutical and preventive purposes.
21
Sprakes, Michael Bramwell. "Clinical and molecular aspects of anti-TNF therapy in Crohn's disease." Thesis, University of Leeds, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.659181.
Abstract:
INTRODUCTION: Crohn's disease (CD) is a, relapsing and remitting inflammatory disorder of the gastrointestinal tract. The pathogenesis of CD is not entirely understood, but may represent a combination of immune, genetic, and environmental stressors. Recently, a number of genes have been discovered that confer susceptibility to CD, many of these functioning in the innate immune system and novel therapies that act on molecules associated with the innate immune system are being developed. The anti-tumour necrosis factor (TNF) therapies, infliximab and adalimumab, are two such treatments, however data relating to the longer-term efficacy and safety of these therapies in CD, along with their cost implications, are limited. NLRP3 is a pathogen recognition receptor which, amongst other ligands, recognises muramyl dipeptide (MDP), the major ligand sensed by NOD2, the first susceptibility gene identified in CD. The NLRP3 inflammasome has recently been associated with inflammation in rheumatoid arthritis (RA) and has been shown to be modulated following infliximab therapy in this condition. AIMS: Firstly, to determine the long-term efficacy, safety and cost implications of anti-TNF therapies in CD, and also to assess the efficacy of switching to a second anti-TNF upon failure or non-response to the initial anti-TNF treatment. Secondly, to investigate the NLRP3 inflammasome and other associated inflammatory molecules in patients with CD at both gene and protein level to analyse if the NLRP3 inflammasome is modulated in CD patients compared to healthy controls, and to determine if the inflammasome is modified following treatment with the anti-TNF therapy, infliximab.
22
Mallon, Patrick William Gerard School of Medicine UNSW. "Clinical and molecular aspects of HIV-associated lipodystrophy." Awarded by:University of New South Wales. School of Medicine, 2006. http://handle.unsw.edu.au/1959.4/33048.
Abstract:
HIV-associated lipodystrophy (HIVLD) syndrome is a condition comprising abnormalities in distribution of body fat and metabolism of lipids and glucose that arises in HIV-infected patients on long-term antiretroviral therapy. This thesis describes clinical research into aspects of the natural history and treatment of HIVLD, as well as molecular research into its pathogenesis centred on subcutaneous adipose tissue. Results demonstrate HIVLD to be a treatment-induced syndrome characterised by initial gains in body fat followed by selective, progressive loss of limb fat. Exposure to thymidineanalogue nucleoside reverse transcriptase inhibitors (tNRTI) induces lipoatrophy through mitochondrial dysfunction of which inhibition of mitochondrial RNA expression, rather than mitochondrial DNA depletion, is an early feature. Mitochondrial dysfunction is associated with decreases in expression of peroxisome proliferatoractivated receptor gamma (PPAR??), an adipocyte transcription factor, which helps explain how tNRTI exposure leads to the loss of adipocyte function. Once established, lipoatrophy is characterised by mitochondrial DNA depletion, although this depletion occurs throughout the mitochondrial genome, suggesting an underlying cause other than inhibition of DNA polymerase gamma. HIVLD is a difficult syndrome to treat. Lipoatrophy is resistant to treatment with rosiglitazone, an agonist of PPAR??, which is ineffective in the setting of ongoing tNRTI therapy and mitochondrial dysfunction. Dyslipidaemia is also difficult to treat as use of pravastatin in the setting of ongoing exposure to protease inhibitors results in only modest declines in fasting cholesterol concentrations. Gains in central fat, such as that seen in patients with buffalo hump, are associated with insulin resistance and diabetes, but only occur in a relatively small percentage of treated patients, suggesting a role for genetic factors in its development. Use of strategies such as avoidance of tNRTI in firstline ART, genetic screening to identify those at risk of toxicities and targeted selection of interventions in subgroups of affected patients, may help prevent this syndrome occurring and better treat those patients in which it has already occurred.
23
Xue, Weicheng, and 薛衛成. "Molecular cytogenetic, epigenetic and tissue dynamic study of gestational trophoblastic disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B45015144.
24
Shidrawi, Ray Georges. "Molecular immune aspects of coeliac disease : organ culture and peptide binding studies." Thesis, King's College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243337.
25
Yang, Min, and 杨敏. "Role of regulatory B cells in autoimmune disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48079832.
Abstract:
Although B cells are well-known for their functions in antibody production and antigen presentation, certain B cell subsets have been recently identified as regulatory B cells to modulate immune responses through cytokine production. However, the microenvironmental factors involved in the induction of regulatory B cells remain largely uncharacterized. B cell-activating factor (BAFF), a member of TNF family cytokines produced by myeloid cells, is a key regulator for B cell maturation and function. However, it remains unknown whether BAFF plays a role in modulating the generation of regulatory B cells and how regulatory B cells suppress autoimmune pathogenesis. In this study, treatment with BAFF significantly increased IL-10-producing B cells in culture of mouse splenic B cells, an effect specifically abrogated by neutralization with TACI-Fc. BAFF-induced IL-10-producing B cells showed a distinct CD1dhiCD5+(B10) phenotype. Phenotypic analysis further indicated that these BAFF-induced B10 cells were marginal-zone (MZ)-like B cells. Interestingly, BAFF treatment in vivo also increased the number of IL-10-producingB cells in splenic MZ regions. Moreover, chromatin immunoprecipitation analysis revealed that BAFF activated the transcription factor AP-1 for binding to IL-10 promoter, demonstrating a novel function for BAFF in inducing IL-10 production. Furthermore, those BAFF-induced B10 cells exhibited significant suppressive effects on CD4+T cell proliferation and Th1 cytokine production in culture.
To explore whether these BAFF-induced B10 cells possess a regulatory function in suppressing autoimmune progression in vivo, collagen-induced arthritis (CIA) mouse model was employed. In vitro-expanded B10 cells and other control B cells were intravenously transferred into DBA/1J mice on the day of 2ndcollagen II (CII)-immunization. After adoptive transfer of BAFF-induced B10 cells, CII-immunized mice exhibited a delayed onset of arthritis and substantially reduced severity of clinical symptoms. The pathogenesis of IL-17-producing CD4+T cells (Th17) in the development of arthritis has been well-recognized, which has led me to test the hypothesis whether B10 cells ameliorate the development of arthritis via modulating Th17 cells. During the progression of CIA, IL-10-producing B cells were decreasedwhereasTh17 cells were significantly increased at the acute phase of CIA. Upon transfer of BAFF-induced B10 cells, a substantially reduction ofTh17 cells in both lymphoid organs and inflamed joints were detected. To verify whether B10 cells inhibit Th17 cell generation in culture, CFSE-labeled na?ve CD4+T cells were cocultured with B10 cells in Th17 cell polarization medium. It was found that B10 cells suppressed Th17 cell differentiation via reducing STAT3 phosphorylation and RORt expression. Although adoptive transfer of Th17 cells triggered the development of CIA in IL-17-/-DBA mice, cotransfer of B10 cells with Th17 cells profoundly delayed the onset of delayed the onset of arthritisand remarkably reduced the infiltration of Th17 cells in synovial fluid.
Taken together, I have identified a novel function of BAFF in the induction of IL-10-producing regulatory B cells. My findings that adoptive transfer of BAFF-expanded B10 cells can effectively suppress the development of experimental arthritisin mice via the inhibition of Th17 cell generation may contribute to the development of new therapeutic strategies in treating human rheumatoid arthritis.published_or_final_version
Pathology
Doctoral
Doctor of Philosophy
26
Hung, Ka-lok Victor, and 洪家樂. "The role of astrocytic endothelin-1 in dementia associated with Alzheimer's disease and mild ischemic stroke." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B42181987.
27
Chow, Yan-ching Ken, and 周恩正. "Characterization of the apoptotic properties of severe acute respiratory syndrome coronavirus (SARS-CoV) structural proteins." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B30105493.
28
Slagsvold, Jens Erik. "N-3 Polyunsaturated Fatty Acids in Health and Disease - Clinical and Molecular Aspects." Doctoral thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for laboratoriemedisin, barne- og kvinnesykdommer, 2009. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-5537.
Abstract:
Omega-3 Flerumettede Fettsyrer og Helse – Kliniske og Molekylære Aspekter Omega-3 fettsyrer tilhører gruppen essensielle fettsyrer. Det betyr at vi ikke kan lage dem selv, men at de må tilføres gjennom kosten, hvor de bl.a. finnes i fet fisk, plantefrø, oljer og nøtter. I kroppen brukes de bl.a. som byggesteiner i hjernevev, øyet og cellemembraner, og til å lage en rekke forskjellige signalmolekyler. Studier tyder på at disse fettsyrene kan ha helsebringende effekter på mange områder, deriblant hjerte- og karsykdommer, betennelsestilstander og kreft. Et for lavt inntak av omega-3 fettsyrer er skadelig. Dagens metoder er ikke ideelle for å påvise for lavt omega-3 kostinntak. Vi har derfor undersøkt om måling av genuttrykket av Δ-6 og Δ-5 desaturaser, som er viktige i omdannelsen av fettsyrer, kan brukes som en markør på omega-3 ernæringsstatus. Vi fant at hvite blodceller i cellekultur oppregulerte genuttrykket av desaturasene når omega-3 fettsyrer manglet. Tilsvarende fant vi at genuttrykket av desaturasene var høyere hos friske forsøkspersoner som ikke spiste fiske enn hos dem som spiste fisk. Denne forskjellen forsvant etter to uker med omega-3 tilskudd. Dette indikerer at genuttrykket av desaturasene er regulert av kostinntaket av omega-3 fettsyrer, men det trengs ytterligere studier for å fastslå om dette kan benyttes diagnostisk til å påvise et for lavt kostinntak av disse essensielle fettsyrene. Flere befolkningsstudier viser at et høyt inntak av omega-3 fettsyrer er assosiert med lav forekomst av visse typer kreft. Dette er best dokumentert for bryst-, prostata- og tykktarmskreft. I cellekultur hemmer omega-3 fettsyrer vekst av kreftceller og gir programmert celledød (apoptose). Imidlertid er de molekylære mekanismene involvert uklare. Studier av genuttrykket til humane leukemiceller (HL60) behandlet med omega-3 fettsyren EPA, viste aktivering av et signalspor kalt ufoldet protein respons (UPR). Dette er en normal stress- og forsvars respons som gir cellene en mulighet til å gjenopprette likevekten og reparere skader før de fortsetter normal cellesyklus. Dersom stresset er for stort kan cellen gå i apoptose. Endringer i kalsiumnivåer i cellen kan utløse UPR. E2R2 celler, en klon av HL60 celler, er motstandsdyktige mot visse endringer i kalsiumnivået. De var mindre følsomme for EPA, og fikk ikke aktivert UPR responsen. Det er derfor sannsynlig at den veksthemmende effekten til EPA skyldes endringer i kalsiumlikevekten, som igjen aktiverer UPR responsen. Vi undersøkte også hvordan fettsyren DHA hemmer vekst av ondartede tykktarmskreftceller (SW620). Analyser av gen- og proteinutrykk viste at flere målproteiner for cellegift i kreftbehandling ble påvirket gunstig. I motsetning til cellegift, er omega-3 ufarlig og uten bivirkninger. Resultatene indikerer at omega-3 kan ha en plass i kreftbehandling, for eksempel i kombinasjon med dagens terapimetoder. Flere studier er nødvendige for å fastslå om behandling med omega-3 kan redusere bruken og/eller øke effekten av konvensjonell kreftbehandling. De foreløpige resultatene synes imidlertid allerede nå å kunne gi grunnlag for å anbefale kreftpasienter omega-3 tilskudd.
29
Shehab, Gaber Mohamed Gomaa. "Molecular aspects of resistance to late blight disease in potato (Solanum tuberosum L.)." Thesis, Durham University, 2002. http://etheses.dur.ac.uk/4032/.
Abstract:
Diseases caused by micro-organisms are still a major threat to the agro-industry worldwide. Diseases not only have negative effects on crop yields, but also they can affect the quality of crops post-harvest. Genetic engineering is one of several strategies that have been developed to control plant diseases and to enhance plant disease resistance to pathogens. Although some genetic strategies have provided plants with enhanced disease resistance, some pathogens can easily overcome this resistance by rapid evolution resulting in a lack of durability in the field. The oomycete Phytophthora infestans, the causal pathogen of late blight disease of potato, is an example of a crop pathogen that causes a major problem in one of the most important crops worldwide. Many efforts have been made trying to control this pathogen including chemical controls and genetic engineering, but unfortunately it remains a severe problem and the control measures are rarely very successful. Due to the complexity of this pathogen, and to limit the need for chemical control, breeding programmes to incorporate durable forms of genetic resistance are crucially needed. Although, this type of resistance is believed to be effective against all known races of P. infestans and provide in additional some level of general resistance, until now the genetic bases of this type of resistance is still unknown and the molecular mechanisms poorly understood. This project set out to isolate and identify gene sequences that are induced during the compatible interaction between cultured potato plants and P. infestans, specifically those leading to the establishment of durable resistance. It was demonstrated that the potato variety Stirling is capable of developing this type of resistance as judged by the development of resistant shoots during the interaction with Phytophthora. These shoots showed very strong resistance not only to Phytophthora but also to other potato pathogens (R. solani and F. sulphureum) even after two generations of culturing the plants in the absence of the pathogen. The fast production of ROS and the tight deposition of callose surrounding the hypersensitive cells, which deprive the pathogen of nutrients and limit pathogen growth to a small region of the plant, may be important factors in the success of the durable plants in defending themselves against the pathogen attack.
30
Tong, Chun-kit Benjamin, and 唐俊傑. "Molecular mechanism of disrupted capacitative calcium entry in familial Alzheimer's disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/205870.
Abstract:
Presenilin (PS) is the catalytic subunit of the gamma-secretase which is responsible for the cleavage of amyloid precursor protein to form beta amyloid (Aβ). Mutations in PS cause familial Alzheimer’s disease (FAD) by increasing the Aβ plaques formation in the brain and thereby induce neurodegeneration. Apart from this, FAD-linked PS mutations have been demonstrated to disrupt cellular calcium (Ca2+) homeostasis. Ca2+is a vital secondary messenger that involved in various neurophysiological functions, including memory, learning, and neuroplasticity and mounting evidence suggesting that Ca2+dysregulation associated with PS mutations may play a proximal role in the AD pathogenesis. Yet, the molecular mechanism for Ca2+dysregulation in AD remains debatable. It has been reported that cellular Ca2+homeostatsis can be disrupted in various ways.
On the one hand, mutant PS has been demonstrated to exaggerate Ca2+release from the endoplasmic reticulum (ER) through different pathways. On the other hand, attenuatedCa2+influx from the extracellular medium through the capacitative Ca2+entry (CCE) pathway has also been reported to bring about cellular Ca2+disruption. However, the molecular mechanism for the PS mutation-mediated CCE deficits is largely unknown. For this reason, the objective of the current study is to elucidate the underlying molecular mechanism for attenuated CCE in AD.
In this study, human neuronal cell line SH-SY5Y is employed as a cellular model to investigate the effect of wild-type or FAD-linked PS1 mutation on CCE pathway. Using single cell Ca2+imaging technique, significant CCE deficits was observed in SH-SY5Y stably expressing FAD-linked PS1mutation, PS1M146L. Interestingly, this CCE attenuation in PS1 mutant expressing cells was not mediated by the down-regulation of STIM1 and Orai1 expression, the known essential molecular players in the CCE pathway. Instead, co-immunoprecipitation and proximity ligation assay have suggested a physical interaction between PS1 and STIM1 proteins. Moreover, a putative gamma-secretase mediated STIM1 cleavage was discovered by western blotting. In addition, confocal imaging showed that PS1M146L significantlyreduceSTIM1 puncta formation and ER translocation followed by the activation of CCE pathway by ER Ca2+store depletion with thapsigargin. This indicated that mutant PS1 attenuates CCE by affecting STIM1 oligomerization or its recruitment with Orai1. Taken together, our results suggested the negative regulatory role of PS on CCE pathway and hypothesized the molecular mechanism of CCE where FAD-linked PS mutation is perceived as a gain-of-function mutation and enhanced the negative impact on STIM1 to inhibit Ca2+entry.This hypothetic model provides new insights into the molecular regulation for CCE pathway and the identification of the interacting domains between PS1 and STIM1 may suggest novel targets for the development of therapeutic agents that help to treat the disease.published_or_final_version
Physiology
Master
Master of Philosophy
31
Claude, Bayingana. "A molecular investigation of the prevalence of suspected periodontopathogens and their association with preterm birth." Thesis, University of the Western Cape, 2010. http://etd.uwc.ac.za/index.php?module=etd&action=viewtitle&id=gen8Srv25Nme4_7812_1373278598.
Abstract:
More than 20 million infants in the world (15.5 % of all births) are born with low birth weight. Ninety-five % of them are in developing countries. Oral colonization of Gramnegative anaerobes has
been implicated as a risk factor for preterm delivery of low birth weight (PLBW) infants. The objective of this study was to investigate the association between periodontal pathogens and pre-term
delivery of low birth weight (PLBW) infants. The study sample included 200 randomly selected women admitted to the department of obstetrics-gynecology of the teaching hospital of Butare in
Rwanda. Mothers were asked to complete a questionnaire in order to identify factors which might pose a health risk to them and their infants. Gingival crevicular fluid (GCF) was collected from each quadrant of the mother&rsquo
s month (using paper points) within 24 hours of delivery. Ten ml of foetal cord serum samples were collected at delivery and 10 ml of maternal serum samples were
collected within 48 of delivery. GCF was examined by PCR for the presence of 5 periodontopathogens and ELISA was used for the evaluation of cytokines (IL-6 and IL-10) and immunoglobulins (IgM, IgG) in foetal cord and maternal blood against the periodontopathogens. P. intermedia showed significant associations either on its own or in combinations with most indicators of
periodontal disease used in this study, while Aa and members of the red complex were significantly associated with gum bleeding and reduced frequency of tooth brushing. A strong association
between PLBW and maternal and foetal cord serum sample levels of IL-10 was observed. Also, a good association was observed between PLBW and FCB sample levels of IL-6. Significant
associations were observed between PLBW and maternal IgG against the different peridontopathogens. The findings of this study may suggest that the levels of maternal IgG and foetal IgM
against the different periodontopathogens are associated with dissemination of maternal periodontopathogens to the foetus thereby illiciting an inflammatory response which contributes to
PLBW.
32
Alvarenga, Leila da Silva. "Detecção e caracterização molecular do herpesvírus humano tipo 6 (HHV-6) em tecido gengival de pacientes acometidos por doença periodontal." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/42/42132/tde-24112008-174425/.
Abstract:
Análise: Estudos recentes têm sugerido que os herpesvírus podem estar envolvidos na ocorrência e progressão de diferentes formas de doença periodontal. Objetivos: O objetivo do presente estudo foi investigar a presença de herpesvírus HHV-6 em biópsias gengivais de pacientes afetados por periodontite crônica e verificar a variabilidade genética das amostras positivas para HHV-6 (HHV-6 A e HHV-6 B). Como controle, biópsias gengivais de sujeitos periodontalmente saudáveis foram analisadas. Materiais e Métodos: Biópsias gengivais foram colhidas de 60 voluntários: 30 casos afetados por periodontite crônica e 30 casos periodontalmente saudáveis. Cada caso contribuiu com 1 biópsia envolvendo o epitélio e tecido conjuntivo da bolsa periodontal contendo profundidade a 5mm e apresentando sangramento à sondagem após o exame clínico; a outra biópsia controle foi concedida de local com profundidade clínica de sondagem a 3mm não apresentando sangramento. Para extração e purificação do DNA viral foi utilizado o kit da Invitrogen® (Charges Switch®g DNA Mini Tissue kit). O DNA extraído foi amplificado utilizando as técnicas de PCR e nested-PCR. Os produtos amplificados foram seqüenciados utilizando o kit Big Dye Terminator (Applied Biosystems). As seqüencias obtidas foram alinhadas com o auxílio do Programa Sequence Navigator e comparadas com amostras padrão do gene bank. Resultados: Após a análise de 60 amostras, seqüências de DNA de HHV-6 foram detectadas em locais periodontalmente saudáveis 4/30 (13,3 %), e em locais com doença periodontal 2/30 (6,7 %); seis produtos positivos da nested-PCR foram seqüenciados e apresentaram homologia para a variante B. Conclusões: O presente estudo demonstrou que o tecido gengival pode agir como reservatório para HHV-6. Nossos dados sugerem que estudos adicionais sejam realizados a fim de consolidar uma associação entre os subtipos de herpesvírus investigados com a doença periodontal destrutiva.Analysis: Recent studies have suggested that the herpesvirus may be involved in the occurrence and progression of different forms of periodontal disease. Objectives: The purpose of this study was to investigate the HHV-6 herpesvirus presence in gingival biopsies of patients affected by chronic periodontitis and to ascertain the positive samples genetic variability for HHV-6 (HHV-6A and HHV-6B). As a control, biopsies of gingival periodontally healthy subjects were examined. Materials and Methods: gingival biopsies were taken from 60 volunteers: 30 cases affected by chronic periodontitis and 30 cases periodontally healthy. Each case contributed with 1 biopsy involving the epithelium and connective tissue of periodontal pocket depth containing 5mm and stating the bleeding on probing after the clinical examination; the other control biopsy was granted from local with clinical survey depth of 3mm showed no bleeding. For extraction and purification of viral DNA was used the Invitrogen® kit (Charges Switch ® g Mini Tissue DNA kit). The extracted DNA was amplified using the techniques of PCR and nested-PCR. The amplified products were sequenced using the Big Dye Terminator kit (Applied Biosystems). The sequences obtained were aligned with the aid of the Sequence Navigator Program and compared with standard samples of gene bank. Results: After the analysis of 60 samples, DNA sequences of HHV-6 were found in places periodontally healthy 4/30 (13,3%), and in places with periodontal disease 2/30 (6,7%); six positive products of nested-PCR were sequenced and showed homology for variant B. Conclusions: This study has demonstrated that the gingival tissue may act as a reservoir for HHV-6. Our data suggest that additional studies must be conducted to consolidate an association between subtypes of herpesvirus investigated and the destructive periodontal disease.
33
Julies, Monique G. "Molecular-genetic analysis of Hirschsprung's disease in South Africa." Thesis, Stellenbosch : Stellenbosch University, 2000. http://hdl.handle.net/10019.1/51835.
Abstract:
Thesis (MSc)--Stellenbosch University, 2000.ENGLISH ABSTRACT: Hirschsprung's disease, or aganglionic megacolon, is a common cause of intestinal obstruction in neonates and is associated with the congenital absence of intrinsic ganglion cells in the myenteric and submucosal plexuses of the gastrointestinal tract. The affected area is usually restricted to the distal part of the colon (short segment disease), but total colonic or intestinal involvement occurs in some patients (long segment disease). DNA analysis was performed on samples from 53 unrelated sporadic HSCR patients to search for mutations in RET proto-oncogene, endothelin-B receptor (EDNRB) and endothelin-3 (EDN3) genes. The patients were from different ethnic groups in South Africa, including 29 coloured, 14 white (Caucasian) and 9 black individuals. The origin of 1 patient was unknown. PCR HEX-SSCP analysis of the RET protooncogene revealed one previously described (P973L) and five novel mutations (V202M, E480K, IVS10-2A1G, D771N, IVS19-9Crr), likely to cause or contribute to the HSCR phenotype. Nine polymorphisms were also identified in the RET protooncogene, of which four were novel (IVS6+56deIG, IVS13-29Crr, IVS16-38deIG, X1159) and five previously described (A45, A432, L769, S904, R982). All the mobility shifts detected in the EDNRB gene represented polymorph isms (A60T, S184, 1187, V234, L277, IVS3-6Crr, IVS4+3A1G). No sequence variants were identified in the EDN3 gene. The majority of mutations in the RET proto-oncogene (28.6%) were identified in coloured patients while no mutations were identified in black patients. A mutation in RET was identified in two of 14 patients (14%) presenting with HSCR and Down's syndrome compared to 6 mutations identified in 9 of 39 patients (23%) with only HSCR. The fact that Down's syndrome patients have a high chance of developing HSCR, implies the involvement of modifier gene(s) in a HSCR/Oown's syndrome phenotype. This study demonstrated that, within the South African HSCR patient population, the RET proto-oncogene is the major susceptibility gene, whereas EDNRB and EDN3 may contribute only to a minority of cases. In 81% of patients no disease-causing mutation could be identified, which is in keeping with the heterogeneous nature of HSCR. The identification of mutations in HSCR patients would in future lead to improved and accurate counselling of South African HSCR patients and their families.
AFRIKAANSE OPSOMMING: Hirschsprung se siekte (HSCR), ook bekend as aganglionosis megakolon, is 'n algemene oorsaak van intestinale obstruksie in pasgeborenes en word geassosieer met die kongenitale afwesigheid van intrinsieke ganglion selle, in die miênteries en submukosa pleksus van die gastrointestinale kanaal. Alhoewel die aangetaste deel hoofsaaklik by die distale area van die kolon geleê is (kort segment siekte), kom totale koloniese of intestinale betrokkenheid ook in sommige pasiënte voor (lang segment tipe). Molekulêre ONS analise van 53 nie-verwante Suid Afrikaanse sporadiese HSCR pasiênte (29 kleurlinge, 14 blankes, 9 swartes en 1 individu van onbekende oorsprong) is uitgevoer in die RET proto-onkogeen, endoteel-B reseptor (EDNRB) en endoteel-3 (EDN3) gene. Heterodupleks-enkel string konformasie polimorfisme (HEX-SSCP) analise van polimerase ketting reaksie (PKR) geamplifiseerde produkte van die RET proto-onkogeen het gelei tot die identifikasie van vyf nuwe mutasies (V202M, E480K, IVS10-2A1G, D771N, IVS19-9CIT) en een bekende mutasie (P973L). Vier nuwe polimorfismes (IVS6+56deIG, IVS13-29Crr, IVS16-38deIG, X1159) en vyf bekende polimorfismes (A45, A432, L769, S904, R982) is ook aangetoon. Sewe polimorfismes (A60T, S184, 1187, V234, L277, IVS3-6CIT, IVS4+3A1G) is in die EDNRB geen geïdentifiseer. Geen veranderinge is in die EDN3 geen waargeneem nie. Die meerderheid mutasies waargeneem in die RET protoonkogeen is in die kleurling populasie (28.6%) waargeneem, terwyl geen mutasies in die swart populasie geïdentifiseer is nie. 'n RET mutasie is in twee van 14 (14%) pasiênte met 'n HSCR en Down's sindroom fenotipe waargeneem, in vergelyking met mutasies geïdentifiseer in 9 van 39 pasiënte (23%) met slegs HSCR. Die algemene voorkoms van Down's sindroom met HSCR, impliseer die rol van ander gene in die HSCRI Down's sindroom fenotipe. Die meerderheid mutasies wat aanleiding gee tot die HSCR fenotipe kom voor in die RET proto-onkogeen (19%), terwyl slegs polimorfismes in die EDNRB geen waargeneem is. Geen HEX-SSCP bandpatroon veranderinge is in die EDN3 geen waargeneem nie. Ongeveer 81% van die Suid Afrikaanse HSCR pasiënte was mutasie-negatief wat dui op die heterogene aard van die siekte. In die toekoms sal analise van siekte-verwante mutasies in die RET geen lei tot akkurate diagnose en verbeterde genetiese voorligting van HSCR in die Suid-Afrikaanse populasie.
34
Pinkerton, Mark Neil, and n/a. "The molecular basis of orthodontic tooth movement : cytokine signaling by PDL cells in tension an in vitro study." University of Otago. School of Dentistry, 2007. http://adt.otago.ac.nz./public/adt-NZDU20071207.161056.
Abstract:
The pressure-tension hypothesis is the governing dogma of orthodontic tooth movement. This theory proposes that the application of loads to the crown of a tooth during orthodontic mechano-therapy results in differential site-specific reactionary strains in the para-dental tissues. Briefly, following the application of orthodontic load the bone and periodontal ligament (PDL) on one side of the tooth is placed in compression favoring bone resorption, while on the other side of the tooth they are placed in tension favoring osteogenesis The present in vitro model provides a surrogate for the PDL on the tension side of the tooth during orthodontic tooth movement and aims to identify mechanically induced changes in the expression of osteo-regulatory cytokines in human PDL cell cultures in response to tensile mechanical strain.
Materials and Methods: PDL explants were obtained from pathology free bicuspids of two human subjects following extraction of the teeth for orthodontic purposes. Following serial passage, cells were plated on Uniflex� plates and consigned to either the experimental or control groups. Experimental cells were exposed to a cyclic uniaxial tensile mechanical strain for 6,12 or 24 hours using the Flexercell FX 4000 strain unit. Total RNA was extracted using a two-step procedure and samples were analysed using real-time RT-PCR assays for a range of osteo-regulatory cytokines.
Results: Human PDL cells expressed mRNA for a range of cytokines of known significance to osteogenesis and osteoclastogenesis in response to mechanical stimulation.
Conclusions: The production of osteo-regulatory cytokines by PDL cells in response to mechanical strain suggests that these cells have the potential to contribute to the osseous modeling of orthodontic tooth movement. The presence of osteogenic signalling drive in response to tensile strain tends to support the basic assertions of the pressure-tension hypothesis.
35
Brink, Daan Matthijs van den. "Molecular aspects of Refsum disease and the enzymatic degradation of phytol to phytanic acid." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2005. http://dare.uva.nl/document/79215.
36
Gallego-Beltran, Juan Fernando. "Leptospirosis in Columbian dairy cattle : microbiological, serological, molecular and epidemiological aspects of the disease." Thesis, Royal Veterinary College (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272308.
37
Wang, Hongxia. "Identification of Molecular Markers Linked to X-Disease Resistance in Chokecherry." Diss., North Dakota State University, 2012. https://hdl.handle.net/10365/26565.
Abstract:
X-disease, caused by phytoplasmas, is one of the destructive diseases in stone fruit trees, causing yield loss and poor fruit quality. So far no effective methods are available to control X-disease. X-disease resistance has been first discovered in chokecherry (Prunus virginiana, 2n=4x=32), which is a native woody species of North America. To identify molecular markers linked to X-disease resistance, simple sequence repeat (SSR) markers were used to construct genetic linkage maps for chokecherry and to identify markers associated with X-disease resistance in chokecherry. In this research, three segregating populations of chokecherry were developed by crossing one X-disease resistant (CL) with three susceptible chokecherry lines (a, c, and d), of which the progenies were 101, 177, and 82, respectively. In order to construct a genetic map for chokecherry, 108 pairs of SSR primers were employed from other Prunus species. Additionally, a set of 246 SSRs were developed from chokecherry sequencing by Roche 454 sequencing technology. A total of 354 pairs of SSR primers were used to screen individuals of all three populations. Two software programs, TetraploidMap and JoinMap, were used to construct linkage map based on single-dose restriction fragments (SDRFs) and two parental linkage maps were generated for each population from both software programs. Bulked segregant analysis (BSA) was applied for identification of X-disease resistance markers. As a result, one SSR marker was found to be linked to the X-disease resistance. The set of 246 chokecherry SSRs was later used to test transferability among another 11 rosaceous species (sour cherry, sweet cherry, wild cherry, peach, apricot, plum, apple, crabapple, pear, june berry, and raspberry). As a result, chokecherry SSR primers can be transferable in Prunus species or other rosaceous species. An average of 63.2% and 58.7% of amplifiable chokecherry primers amplified DNA from cherry and other Prunus species, respectively, while 47.2% of amplifiable chokecherry primers can be transferable to other rosaceous species. The genetic information, including genetic map, disease linked marker, chokecherry sequence, and confirmed transferability of the identified chokecherry SSRs to other species, will benefit the genetic research in Prunus and other rosaceous species.
38
Abdullah, Mohd Pu'ad. "Biochemical and molecular studies of some aspects of disease resistance in potato (Solanum tuberosum L.)." Thesis, Durham University, 1999. http://etheses.dur.ac.uk/4859/.
Abstract:
Disease problems in crop plants are still a major threat to the agro-industry worldwide. Various strategies have been developed and evaluated in recent years. One strategy is to use naturally-occurring antipathogen factors such as lysozymes and chitinases in transgenic plants. In the present study, transgenic plants containing chick-egg white lysozyme (Lys 75) have been evaluated for lysozyme production in planta, subcellular localisation, and resistance to some potato pathogens, including Phytophthora infestans and Erwinia carotovora subsp. atroseptica, the two major potato pathogens worldwide. In addition, the evaluation of resistance was also undertaken for transgenic plants carrying other naturally-occurring antipathogen factors including a bean chitinase gene (BCH 35) and a snowdrop lectin gene (GNA 74). In order to accurately quantify the lysozyme production in Lys 75 plants, the turbidimetric lysozyme enzyme assay was optimised. Also, a modified substrate for the enzyme has been developed by covalently linked the Micrococcus lysodeikticus cell wall with a dye, remazol brilliant violet 5R to enable a colorimetric assay of the enzyme. In order to quantitatively assess resistance levels of the transgenic plant, a new method (leaf-bridge bioassay) for conducting and evaluating resistance in planta has been developed. All transgenic plants in tissue culture were tested for resistance using this technique. Evaluation of the progress of infection in detached leaves of Lys 75 showed that lysozyme gave some degree of protection against the bacterial pathogen, Erwinia carotovora subsp. atroseptica and the fungal pathogen, Fusarium sulphureum. Analysis of intercellular fluid from the Lys 75 leaves showed that more than 80% of the total lysozyme expressed in the leaf was located in the intercellular space which is a strategic place to combat pathogen attack. In contrast, the levels of protection in BCH 35 plants were relatively low compared with Lys 75. The progress of infection was delayed in BCH 35 leaves challenged with F. sulphureum only. No resistance at all was observed in GNA 74 to all the pathogens used. All the transgenic potato lines were susceptible to P. infestans. Recently, a new strategy to combat disease problems has been suggested based on a 'durable resistance'. Potato variety Stirling' which shows durable resistance in the field has been used to study the early biochemical and molecular events during elicitation of 'Stirling' cell suspension cultures with an elicitor mix derived from infective units of a compatible strain of P. infestans. For comparison, an elicitor mix from an incompatible strain of P. infestans was also prepared and used. The mixed elicitor comprising zoospore extract, culture filtrate and mycelium homogenate induced defence responses in 'Stirling' cell suspension cultures as judged by the increase in PAL enzyme activity. PAL activity in 'Stirling' ceUs elicited with an elicitor mix derived from an incompatible strain of P. infestans was twice the activity in the compatible interaction. The peak levels in both types of interaction were at 6 h post-elicitation. An oxidative burst was demonstrated also in both types of interactions indicated by rapid release of H(_2)O(_2) into the culture medium. The H(_2)O(_2) level peaked at 2 h post-elicitation in both interactions before being reduced to its normal level at 4 h. The H(_2)O(_2) released during incompatible interaction was twice the levels monitored in the compatible. A subtracted cDNA library of differentially expressed mRNAs during elicitation of 'Stirling' cell suspension cultures with the elicitor mix from a compatible strain of P. infestans was constructed using suppression subtractive hybridisation. Two cDNA clones, STS 42 and STS 52, relevant to the present study were identified and characterised. STS 42 showed high degree of similarity to potato leucine aminopeptidase gene which is induced in response to wounding. Gene expression studies using RT-PCR showed that the mRNA levels of STS 42 increased gradually throughout the 18 h elicitation. STS 51 was identified as a member of the ribonuclease T2 histidine proteins. It showed some degree of similarity to plant ribonucleases involved in self-incompatibility reactions during pollination. It has a site for tyrosine kinase phosphorylation at the hydrophilic region of the sequence and could possibly be involved in phosphorylation during signal transduction. mRNA levels of STS 51 were increased during the first 12 h of elicitation.
39
Yu, Yong Gang. "Molecular genetic analysis of host resistance to soybean mosaic virus." Diss., Virginia Tech, 1994. http://hdl.handle.net/10919/37253.
40
Choi, Wai-yee Junet, and 蔡偉儀. "Serum neopterin for early assessment of severity of severe acute respiratory syndrome and Dengue virus infection." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B32031579.
41
Scholten, II Donald Jay. "Characterizing Tumor Hypoxia and Anoikis Resistance in Human Osteosarcoma| Addressing Critical Aspects of Disease Progression." Thesis, Van Andel Research Institute, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10274900.
Abstract:
Osteosarcoma (OS) is the most common type of solid bone cancer, mainly arising in children and young adults, and remains the second leading cause of cancer-related death in this age group. Chemotherapy resistance underlying latent recurrence and metastasis represent major contributors to poor outcome for many cancer patients especially those with OS. Tumor hypoxia is an essential element intrinsic to most solid tumor microenvironments and is associated with resistance to therapy and a malignant phenotype, while metastatic dissemination is dependent on a cells ability to resist anoikis, i.e., programmed cell death in the absence of attachment to an extracellular matrix. We sought to better characterize hypoxia and anoikis resistance in human OS using established and novel patient-derived OS cells and OS animal models with the long-term goal of identifying and validating targetable signaling pathways. We show that hypoxia-inducible factors (HIFs), canonical proteins associated with the hypoxic response, are present and can be induced in human OS cells. We demonstrate that the Wnt/β-catenin signaling pathway, a key pathway in OS pathogenesis, is down-regulated in response to hypoxia in OS cells, and that this appears to result from both HIF-dependent and HIF-independent mechanisms. Hypoxia promotes resistance of human OS cells to standard chemotherapy, which is mitigated by treatment with Wnt/β-catenin signaling inhibitors. Using an anchorage-independent growth model, we show that anoikis-resistant OS subpopulations have altered growth rates, increased resistance to standard chemotherapies, and display distinct changes in gene expression and DNA methylation. Finally, we validate the use of two FDA-approved epigenetic therapies predicted by expression profiling in both inhibiting anchorage-independent growth and sensitizing anoikis-resistant OS cells to chemotherapy. In summary, despite the heterogeneity of human OS, our work suggests that unique and effectively targetable signaling pathways underlie the phenotypic consequences in response to hypoxia and anoikis resistance.
42
陳蓓華 and Pui-wah Vicky Chan. "Molecular genetics of Hb H disease in Hong Kong Chinese." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B31970904.
43
Rodrigues, Italo Sarto Carvalho 1983. "Análise da diversidade bacteriana associada ao biofilme dentário por polimorfismo de comprimento de fragmentos terminais de restrição (T-RFLP)." [s.n.], 2011. http://repositorio.unicamp.br/jspui/handle/REPOSIP/290618.
Abstract:
Orientadores: Daniel Saito, José Francisco HoflingDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba
Made available in DSpace on 2018-08-18T23:33:02Z (GMT). No. of bitstreams: 1 Rodrigues_ItaloSartoCarvalho_M.pdf: 3160518 bytes, checksum: 533e1e1de47c1a11817a14777f4dcc3e (MD5) Previous issue date: 2011
Resumo: As comunidades bacterianas presentes na cavidade bucal desempenham papel importante no equilíbrio saúde/doença em seres humanos. Nesse sentido, o estudo da composição de microambientes orais pode contribuir para uma melhor precisão no diagnóstico de doenças infecciosas e, consequentemente, para o desenvolvimento de abordagens terapêuticas mais eficazes. A periodontite é uma doença dos tecidos de suporte do dente, caracterizada por resposta imunológica exacerbada do hospedeiro, frente à presença bacteriana no biofilme dentário. A grande diversidade bacteriana observada na cavidade bucal, aliada aos variados quadros clínicos da periodontite, ressaltam a necessidade de investigações mais aprofundadas sobre a composição bacteriana periodontopatogênica. O objetivo deste trabalho é a caracterização da comunidade bacteriana associada ao biofilme periodontopatogênico, pelo uso da técnica de Polimorfismos de Comprimento de Fragmentos Terminais de Restrição (T-RFLP). Amostras de biofilme dentário supragengival e subgengival foram coletadas de 11 pacientes portadores de periodontite. O DNA amostral foi extraído e submetido à Reação em Cadeia da Polimerase (PCR) direcionada ao gene ribossomal 16S, utilizando-se iniciador senso marcado com molécula repórter fluorescente. Os produtos da PCR foram digeridos pelas endonucleases tetraméricas HhaI, MspI e RsaI e os fragmentos terminais de restrição (T-RFs) resultantes foram analisados em um sequenciador automatizado de DNA, gerando diferentes perfis de fragmentos para cada amostra. Ao todo, 19 T-RFs distintos foram detectados com a enzima RsaI (média = 6,4), 61 com MspI (média = 19,3) e 63 com HhaI (média = 16,3). Uma grande variabilidade nos perfis de restrição foi observada, sendo que 51% a 63% dos T-RFs foram detectados em menos de quatro amostras. A predição taxonômica de T-RFs in silico demonstrou a presença de gêneros bacterianos reconhecidamente periodontais, incluindo Actinomyces, Eubacterium, Fusobacterium, Haemophilus, Porphyromonas, Prevotella e Propionibacter. Embora alguns gêneros tenham sido encontrados em todas as amostras avaliadas, as análises de clusterização e estatística multivariada não demonstraram agrupamentos de perfis T-RFLP conforme paciente ou sítio amostral. Os resultados do estudo permitem concluir que a comunidade bacteriana do biofilme periodontopatogênico é bastante variável entre indivíduos, embora possua alguns gêneros predominantes
Abstract: The bacterial communities present in the oral cavity play an important role in maintaining healh/disease equilibrium. In this sense, studying the microbial compostition of the oral environment may contribute to attain a better precision in diagnosis of infectious diseases and, also, to develop efficient therapeutic approaches. Periodontitis is a disease that affects the supporting tissues of the tooth, characterized by a heightened immunologic response to bacteria present in dental biofilm. The broad microbial diversity present in the oral cavity, along with the various clinical features of periodontitis, highlight the necessity of further investigations on the composition of periodontopathic biofilm. The objective of this study is the characterization of the bacterial communities associated with periodontopathic biofilm, by use of the Terminal Restriction Fragment Length Polymorphism (T-RFLP) techique. Supra and subgingival biofilm samples were collected from 11 periodontitis subjects. Total DNA was extracted from the samples and submitted to the Polymerase Chain Reaction (PCR) targeting the 16S rRNA gene, with a fluorescently labeled forward primer. PCR products were digested with the tetrameric endonucleases HhaI, MspI and RsaI, and the resulting terminal restriction fragments (T-RFs) were analyzed in an automated DNA sequencer. In all, 67 T-RFs (mean = 17.3) were detected with RsaI endonuclease, 61 T-RFs with MspI (mean = 19.3) and 19 T-RFs (mean = 6.4) with HhaI. A great variability in the restriction patterns was observed, since 51% to 63% of T-RFs were detected in less than 4 samples, and two T-RFs were exclusively found in supragingival biofilm (p = 0.018). In silico taxonomical prediction of T-RFs demonstrated the presence of well-known periodontal species belonging to the Acinomyces, Eubacterium, Fusobacterium, Haemophilus, Porphyromonas, Prevotella and Propionibacter genera. Although some species were found in all samples, clustering and multivariate statistical analysis did not reveal evident groupings of T-RFLP profiles according to patient or sampling site. The results of this study indicate that the microbiota of periodontopathic biofilm is highly variable among subjects, albeit a core microbial community may be observed
Mestrado
Microbiologia e Imunologia
Mestre em Biologia Buco-Dental
44
Cooper, Natalie R., and University of Lethbridge Faculty of Arts and Science. "Reduced peri-infarct dysfunction with pre-stroke exercise : molecular and physiological correlates." Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2003, 2003. http://hdl.handle.net/10133/215.
Abstract:
The effects of pre-stroke exercise and levesl of brain-derived neurotrophic factor (BDNF) on behavioural and functional recovery were examined following focal cortical ischemic infarct.
Intracortical microstimulation (ICMS) was used to derive topographical maps of forelimb
representations within the motor cortex and ischemia was induced via bipolar coagulation of surface vasculature. One month of excerise prior to ischemia significantly increased the
amount of peri-infarct movement represnetations and initiates vascular changes within motor
cortex. Further, this exercise-induced preservation of peri-infarct movement representations is associated with behavioural recovery and is dependent on BDNF levels in the motor cortex. These results provide further support for the idea that endurance exercise prior to stroke
may enhance functional and behavioural recovery.140 leaves : ill. (some col.) ; 29 cm.
45
Millet, Jean Kaoru Guillaume. "Host cell susceptibility to human coronavirus infections." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B44548102.
46
Talegaonkar, Sonia S. "The Role of Human MSC Derived Exosomes in the Treatment of Periodontal Diseases." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4969.
Abstract:
Periodontal disease affects 47% of Americans over 30. Characterized by microbial dysbiosis and unregulated inflammation, severe periodontitis causes degradation of bone and soft tissue around teeth. Current treatments have limited regenerative outcomes and frequent reinfection by harmful bacteria. Human mesenchymal stem cells (hMSCs) have been shown to promote wound healing and tissue regeneration. Many therapeutic benefits of hMSCs are due to their secretome products, like exosomes. Our long-term goal is to develop periodontal therapies with hMSC exosomes. The objectives of this study were to determine the effect of hMSC-derived exosomes on cellular activity of hMSCs and investigate whether hMSC exosome treatment reduces pro-inflammatory cytokine production in LPS-activated RAW264.7 cells. The specific aims of this study were: 1) Determine the characteristics of hMSC-derived exosomes, 2) Determine the biological effect of exosomes on cellular activity of hMSCs, 3) Determine whether exosomes treatment can inhibit cytokine production in activated RAW264.7 cells, and 4) Determine the role of exosomal miRNA in pro-inflammatory cytokine production of RAW264.7 cells. To investigate, exosomes were first harvested from hMSCs culture media through ultracentrifugation. Exosomes were then observed under a transmission electron microscope (TEM) and assessed for surface markers using Western Blot. A transwell migration assay was used to evaluate the chemotactic effect of exosomes. To study the effect of exosomes on stem cell proliferation, exosomes were administered to hMSCs. The immunogenicity of MSC exosome was also evaluated. After 72 hours, cells were lysed and DNA was measured. To study anti-inflammatory effects of exosomes, LPS stimulated RAW264.7 cells were treated with exosomes. Interleukin-6 (IL-6) and tumor necrosis factor alpha (TNFα) levels of supernatant were measured by ELISA. To study exosomal miRNA, exosomal miRNAs were overexpressed in RAW264.7 cells and these cells were stimulated with LPS. IL-6 and TNFα were measured by ELISA. TEM images showed that exosomes are nano-sized vesicles (~100 nm). Western blot images showed that CD63 and CD81 are enriched in exosomes compared to total cell lysates. Exosome treatment increased cell proliferation and migration in hMSCs. At the doses that are chemotactic and mitogenic, MSC exosomes had minimal effect on the inflammatory cytokine IL-6 production. Treatment with exosomes significantly decreased IL-6 and TNFα production in RAW264.7 cells activated by LPS. Transfecting RAW264.7 cells with exosomal miR-760 significantly decreased IL-6 production, but had minimal effect on TNFα. Our results indicate that exosomes have a pleiotropic activity, which includes stimulating stem cell migration and proliferation, and mitigating the inflammatory response. Therefore, hMSC exosome delivery is promising for the treatment of periodontal diseases.
47
Lu, Qian, and 陸茜. "Expression and regulation of human {221}-defensins in gingival epithelia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B36613708.
48
Dufresne, Philippe J. "Development and validation of molecular markers for the detection of disease resistance alleles in Lactuca sativa." Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=78352.
Abstract:
In this study, RAPD (Randomly Amplified Polymorphic DNA) and SCAR (Sequence Amplified Characterized Region) markers found within 5 centiMorgans of known disease resistance loci in L. sativa were tested for their potential use in MAS. Out of thirty RAPD and SCAR markers evaluated, ten were found to be reliable predictors of disease resistance or susceptibility across a wide range of commercial and reference cultivars. Direct sequencing of seven selected markers did not reveal any significant similarity with known sequences. Three SNPs (Single Nucleotide Polymorphism) associated with two markers found in close proximity to corky root (cor) and Lettuce mosaic virus resistance (mo12) genes were identified. This information was used in the development of a non-electrophoresis PCR-based assay called FRET (Fluorescence Resonance Energy Transfer) hybridization probes assay.
49
Stovall, Kirk Hiatt. "Partial restoration of cell survival by a human ependymin mimetic in an in vitro Alzheimer's disease model." Link to electronic thesis, 2006. http://www.wpi.edu/Pubs/ETD/Available/etd-082106-133513/.
50
Li, Sze-ming Kenneth, and 李思銘. "Bat as the animal origin of SARS-CoV and reservoir of diverse coronaviruses." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B42182463.