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Published: 4 June 2021
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1

Smajlovic, Dzenan. "Bestämning av FTO (Fat mass and obesity associated gene) polymorfism." Thesis, University of Kalmar, School of Pure and Applied Natural Sciences, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:hik:diva-804.

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Vetenskapen har på senare år försökt fastställa de olika orsaker som leder till fetma. Det är känt att högt energiintag och för lite motion för eller senare hos de flesta individer resulterar i fetma. Det som kan konstateras är att ärftlighet i samspel med miljön vi lever i och påverkas av kan vara den huvudsakliga orsaken till en rad sjukdomar inklusive fetma. På senare år har forskare upptäckt olika gener som på ett eller annan sett är involverade i ämnesomsättningen. En sådan gen är ”fat mass and obesity associated gene”, FTO. Denna gen återfinns på kromosom 16 och har en storlek på 410 kilobaspar. Genen består av nio kodande områden, exoner, och 8 icke kodande områden, introner. Genens funktion är inte fastställd men den tycks både reglera ämnesomsättningen och lipolysen i kroppen. Tidigare studier har konstaterat att en specifik polymorfi i nukleotid rs9939609 medför ökad risk för sjuklig fetma. Uppsättningen som förekommer i nukleotiden uttrycks med A och T. Där dubbel uppsättning av A- allelen klassas som ärftlig risk för fetma. Syftet med detta examensprojekt är att bestämma polymorfi hos FTO genen med hjälp av två olika pyrosekvenserings- baserade metoder. Metod 1 bygger på extraktion av DNA från helblod, sedan amplifiering med PCR och slutligen pyrosekvensering. Metod 2, som jämfördes med metod 1, bygger på PCR direkt på helblod och pyrosekvensering. Blod från 97 friska individer analyserades. Med metod 1 konstaterades förekomst av följande genotyper i provmaterialet, 11 A/A homozygota, det vill säga har riskallelen för fetma i dubbeluppsättning, 50 A/T heterozygota och 36 T/T, vildtyp, som står för minskad ärftlig risk för fetma respektive ingen alls. Med metod 2 som skulle testas, visade sig resultatet överensstämma med metod 1. Med metod 2 erhölls följande resultat 11 A/A, 49 A/T och 34 T/T. Med metod 2 kunde inte 3 prov analyseras. Slutsatsen som kan dras utifrån studien i detta projekt är att metod 2 är likvärdig metod 1 ur analyssynpunkt. Metod 2 är arbetsbesparande tidsmässigt och även billigare då DNA extraktionssteget inte behöver genomföras.

2008:BL10


Science has for a long time looked for an answer for obesity. Obesity is often explained as the problem of the energy we eat and don’t use, but obesity might also have  hereditary causes, where specific genes might play an important role. One of the recent genes found is the fat mass and obesity associated gene, FTO, which is located  on chormosome 16 and has a size of 410 kilobasepairs. The gene is composed of nine exons and eight introns. The function of the gene is not known in detail, but studies has indicated that the gene could play a part in regulating the metabolism and fat cell lipolysis. The purpose with this examination degree project was to compare two methods for analysis of polymorphism in the FTO gene. Method 1 is based on DNA purification from whole blood, amplification with PCR, and finally detection using pyrosequencing. In method 2 PCR is performed on whole blood  directly without prior DNA purification. Pyrosequencing was used with this method also to detect the polymorphism. Earlier studies have shown that theSNP (single nucleotid polymorphism) rs9939609, is associated with increased risk for obesity. Results obtained using method 1 were, 11 individuals had the A/A genotype, 50 was heterozygous (A/T), and 36 the wild type form (T/T), that is not associated with an increased risk for obesity. With method 2, the same result as with method 1 was obtained for the 94 samples of blood analyzed; 11 A/A, 49 A/T and 34 T/T were obtained. Remaining three samples of the 97 analyzed, failed in the pyrosequencing with method 2.

The conclusions  with this degreeprojcet were that method 1 and 2 gave the same results. Method 2 is recommended as it is faster and less expensive, as no prior DNA purification is needed.

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2

Laber, Samantha. "Deciphering the function of obesity-associated regulatory elements within FTO." Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:5608bad0-f089-408b-bf88-792e875f0326.

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Genome-wide association studies have repeatedly shown that the strongest association with obesity arises from variants in the first intron of FTO. The intronic FTO variant rs1421085 is within an adipocyte-specific enhancer and that risk allele carriers have increased IRX3 and IRX5 expression in early adipogenesis (Claussnitzer et al., 2015). Additionally, the same human risk variant was linked to decreased AKTIP, RPGRIP1L and FTO expression in iPSC-derived neurons (Stratigopoulos et al., 2016). These data point towards several likely causal transcripts and tissues at the FTO locus and essentially, several likely mechanisms. Importantly, whether any of the high-risk variants at the FTO locus has any effect on the organismal level has not been addressed so far. The aim of my DPhil project was to use novel gene manipulation strategies in vivo to mechanistically dissect the Fto regulatory circuitry in mouse to pinpoint causal transcripts their effector tissues and to unravel their physiological role in body weight regulation . Using publicly available as well as my own genomic data (ATAC-seq) revealed that the intronic FTO regulatory element in human adipocytes is conserved in mouse pre-adipocytes. Manipulation of the corresponding motif in mouse (by deleting 82 nucleotides at the mouse orthologous region around rs1421085) resulted in depot- and sex-specific alteration of target genes Irx3 and Irx5 in pre-adipocytes. In addition to recapitulating many of the human findings in mouse, my results further unravelled a new level of regulatory complexity at the FTO/Fto locus. When these mutant mice were put on a high fat diet, I found a reduction on overall fat-mass that could be linked to altered mRNA levels of Irx3 and Irx5 in pre-adipocytes. Using a number of genetic techniques, I further showed that Irx3 regulates several processes during adipocyte development, amongst which is modulation of mitochondrial function. In summary, my findings provide new insight into how variants in FTO intron 1 affect adipocyte development and more specifically how IRX3 affects early adipocyte differentiation.
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3

Cheung, Man Ka. "Investigating the cellular function of the fat mass and obesity associated (FTO) protein." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608074.

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4

Stasiak, Lukasz. "Functional analysis of the fat mass and obesity associated (Fto) gene and protein." Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:74abbb87-26f6-423d-b231-2d910f707bcd.

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Genome wide association studies have shown that common variants in the human fat mass and obesity-associated (FTO) gene predispose to obesity and increased fat mass. Mice globally lacking Fto are lean, while mice globally overexpressing Fto have increased body weight due to increased fat mass. FTO protein was shown to localise to the nucleus and demethylate ssDNA and ssRNA. However, the mechanisms by which FTO mediates its effects on body phenotype remain unknown. In this thesis, I found that native FTO can be detected in both the nucleus and the cytoplasm during interphase, and that nuclear FTO was exported through the nuclear membrane during early prophase of the mitotic cell division. I developed co-immunoprecipitation (Co-IP) protocol to pull-down native FTO and identified a large number of new candidate binding partners (CBPs). Computational analysis predicted a role for FTO, and many CBPs, in RNA post-transcriptional modification and processing. I confirmed that the E3 ubiquitin-protein ligase TRIM21 interacts with FTO in multiple mouse tissues and binds FTO through its SPRY domain. Importantly, TRIM21 ubiquitinated FTO which did not lead to its degradation. FTO partially co-localised with TRIM21 and the decapping enzyme DCP2 in mRNA processing bodies (p-bodies). Overexpression of TRIM21 led to the accumulation of FTO outside the nucleus, but was reversed when both proteins were overexpressed. Additionally, I created a muscle specific Fto knock-out mouse model and found that lack of FTO in muscle did not result in the body composition phenotype reported in global Fto knock-out mice. Taken together, FTO can function in both the cytoplasm and the nucleus, where it interacts with TRIM21 which ubiquitinates FTO and potentiates its cytoplasmic localisation. Moreover, function of FTO in muscle does not mediate the obesity phenotype in mice.
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5

Moens, Thomas Grover. "Molecular mechanisms of pathogenesis in Drosophila models of C9orf72 mutation associated ALS/FTD." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10046295/.

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A GGGGCC hexanucleotide repeat expansion within the C9orf72 gene is the most common genetic cause of both amyotrophic lateral sclerosis and frontotemporal dementia (ALS/FTD). Toxicity has been proposed to be due to loss of function of the gene, or by a toxic gain of function, mediated either by the transcription of repetitive sense and antisense RNA molecules, or by translation of RNA into five repetitive dipeptide proteins (DPRs) via repeat associated non-ATG initiated translation. In order to fully assess the role of sense and antisense RNA in vivo, Drosophila models were created where expression of sense or antisense RNA was induced whilst suppressing the formation of DPRs. Despite the formation of cardinal pathological features (RNA binding protein sequestering intranuclear RNA foci) toxicity was not observed in these models suggesting that repeat RNA plays a limited role in disease pathogenesis. When individual DPRs are expressed in Drosophila neurons a strong toxicity is induced by the arginine containing DPRs (poly-GR and poly-PR). To gain insight into the mechanism(s) by which this toxicity occurs, the protein-interactome of these DPRs was investigated in vivo using novel transgenic Drosophila that inducibly express affinity tagged DPR constructs, with identification of interacting proteins using mass spectrometry. In parallel, inclusions of dipeptide proteins were laser-capture microdissected from patient brain tissue and enriched proteins identified by mass spectrometry. The overlap of these datasets suggested that translation may be impaired by the arginine-containing DPRs and methods were adapted to assess the rate of translation in adult Drosophila brains. In parallel, enzymelinked immunosorbent assays (ELISAs) were developed against poly-GR and an abundant non-toxic DPR poly-GP. Measurement of these proteins was performed in various model systems (transfected immortalised cell lines, induced pluripotent stem cell derived neurons, Drosophila models) to confirm the validity of the assays and the potential therapeutic value of interventions.
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6

ru, neretin@main mccme rssi. "Groups of Vassalomorphisms and Hilbert Spaces Associated with Trees." ESI preprints, 2001. ftp://ftp.esi.ac.at/pub/Preprints/esi1047.ps.

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7

McMurray, Fiona. "Investigating the role of the fat mass and obesity associated gene (Fto) in obesity." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:d7b76f58-6206-47fc-a208-7eeefac7fe27.

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In 2007, a genome wide association study identified a SNP in intron 1 of FTO with increased BMI. Homozygous risk allele carriers are on average three kg heavier than those homozygous for the protective allele. Mouse models have been made, including a conditional knockout, which is lean when globally expressed, as well as a conditional overexpression allele, which has increased body weight when globally expressed. The results from these and other studies suggest that the FTO SNPs lead to weight gain by increasing FTO activity and/or expression. Adult inactivation of Fto using the tamoxifen inducible Cre demonstrated that removal of Fto may be as deleterious as overexpression, with the adult knockout mice having increased fat mass and decreased lean mass. It also supported the role FTO plays in development as adult inactivation of Fto did not increase mortality rates as seen in the global Fto-/- pups. This study also revealed the importance of effective energy expenditure analysis in the mouse. I have confirmed a link between Fto-/- and increased mortality, which may be caused by alterations to developmental processes. Fto-/- reduces cilia formation in MEFs and results in dysregulated cilia formation in specific tissues in Fto-/- embryos. Levels of FTO also appear to affect adipogenic differentiation, which could be due to altered WNT/β-CATENIN signalling. Pharmacological inhibition of FTO was a success in vitro and a compound screen identified FG2216, which could be used in vivo to inhibit FTO. The in vivo effects of FG2216 at 60 mg/kg/2days did not affect body weight or composition in the mouse. My research suggests that there is dysregulation of gut hormones and neuronal signalling pathways in the FTO overexpression mice, which could cause the hyperphagia and increased body weight. These studies add to our current knowledge of FTO function, and suggest a role for FTO in control of body composition, development, and satiety signalling.
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8

Church, Christopher David. "Mouse models for the functional analysis of the fat mass and obesity associated gene FTO." Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534152.

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9

Dietrich, Kerstin. "Molekulare Evolution der metabolisch relevanten Gene MTNR1B (Melatoninrezeptor 1B) und FTO (Fat Mass and Obesity Associated)." Doctoral thesis, Universitätsbibliothek Leipzig, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-104580.

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Die hier vorliegende Arbeit zeigt die molekulare Evolution des Melatoninrezeptor 1 B-Gens (MTNR1B) und des Fat Mass and Obesity Associated-Gens (FTO). Für beide Gene wurden in genomweiten Assoziationsstudien (GWAS) Varianten entdeckt, welche zu der Entwicklung einer Adipositas bzw. deren Folgeerkrankungen beitragen können. So wurde für Einzelbasenaustausche (SNPs) im MTNR1B (rs10830963, rs4753426) eine Verschlechterung der Nüchternglukose sowie der Insulinausschüttung gezeigt. Zudem wurde für die Allelfrequenz des rs4753426 C-Allels ein Zusammenhang mit der täglichen Sonnenscheindauer beschrieben. Im FTO wurde eine (tagging) Variante im ersten Intron identifiziert (rs9939609), welche einen erhöhten Körpermasseindex (BMI) zu vermitteln scheint und robust repliziert werden konnte. Zusätzlich konnte in den Sorben, einer in der Lausitz ansässigen Volksgruppe, eine Variante im dritten Intron (rs17818902) beschrieben werden, die ein zusätzliches, stärkeres Assoziationssignal mit einem erhöhten BMI zeigte. Dies führte zu der Fragestellung, ob MTNR1B und FTO einer Konservierung unterlegen sind. Zudem interessierten populationsspezifische Unterschiede, um die Untersuchungen in den Kontext der Hypothese des sparsamen Genotyps stellen zu können. Demnach haben Individuen mit einer genetischen Veranlagung, die ihnen eine effizientere Energiespeicherung ermöglicht, zu Zeiten von Nahrungsmangel einen Fitness-Vorteil gegenüber Nicht-Trägern. Die Konservierung zwischen den Spezies wurde mit Phylogenetic Analysis by Maximum Likelihood (PAML) betrachtet, eine Analyse die auf dem Verhältnis von nichtsynonymen zu synonymen Basenaustauschen innerhalb einer kodierenden Sequenz beruht. Die Selektion innerhalb bzw. zwischen menschlichen Populationen wurde anhand verschiedener populationsgenetischer Variablen näher beleuchtet. Sowohl für MTNR1B als auch für FTO konnte gezeigt werden, dass sie über die betrachteten Spezies im Durchschnitt stark oder sehr stark konserviert sind, was die physiologische Relevanz dieser Gene untermauert. Für MTNR1B zeigte sich zudem, dass es auf dem Ast zum Menschen nicht konserviert, sondern positiv selektioniert ist. Dies kann als Anzeichen für durch die Umwelt bedingte Einflüsse gedeutet werden. Essentielle Residuen des Rezeptors sind jedoch auch hier hochgradig konserviert. Die populationsgenetischen Variablen implizieren bei beiden Genen eine nicht-neutrale Selektion. Während sich beim MTNR1B insbesondere populationsspezifische Unterschiede anhand des Fixierungsindex Fst zeigten, konnten für FTO marginal signifikante Korrelationen zwischen der Konservierung der Haplotypen und der Stärke der Assoziation mit BMI in den Sorben gezeigt werden. Für beide Gene kann die Hypothese des sparsamen Genotyps nicht prinzipiell ausgeschlossen werden, allerdings sind weitere Untersuchungen diesbezüglich von Nöten.
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Killgore, William D. S., Ryan Smith, Elizabeth A. Olson, Mareen Weber, Scott L. Rauch, and Lisa D. Nickerson. "Emotional intelligence is associated with connectivity within and between resting state networks." OXFORD UNIV PRESS, 2017. http://hdl.handle.net/10150/626076.

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Emotional intelligence (EI) is defined as an individual's capacity to accurately perceive, understand, reason about, and regulate emotions, and to apply that information to facilitate thought and achieve goals. Although EI plays an important role in mental health and success in academic, professional and social realms, the neurocircuitry underlying this capacity remains poorly characterized, and no study to date has yet examined the relationship between EI and intrinsic neural network function. Here, in a sample of 54 healthy individuals (28 women, 26 men), we apply independent components analysis (ICA) with dual regression to functional magnetic resonance imaging (fMRI) data acquired while subjects were resting in the scanner to investigate brain circuits (intrinsic resting state networks) whose activity is associated with greater self-reported (i.e. Trait) and objectively measured (i.e. Ability) EI. We show that higher Ability EI, but not Trait EI, is associated with stronger negatively correlated spontaneous fMRI signals between the basal ganglia/limbic network (BGN) and posterior default mode network (DMN), and regions involved in emotional processing and regulation. Importantly, these findings suggest that the functional connectivity within and between intrinsic networks associated with mentation, affective regulation, emotion processing, and reward are strongly related to ability EI.
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Dehmoune, Jalal Decruppe Jean-Paul. "Rhéoépaississement de systèmes auto-associatifs de la famille CnTAB." [S.l.] : [s.n.], 2007. ftp://ftp.scd.univ-metz.fr/pub/Theses/2007/Dehmoune.Jalal.SMZ0734.pdf.

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12

Hasenkamp, Laura-Carolin [Verfasser], and Christian [Akademischer Betreuer] Haass. "ALS and FTLD associated FUS in zebrafish : investigating disease mechanisms in vivo / Laura-Carolin Hasenkamp. Betreuer: Christian Haass." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2016. http://d-nb.info/109991051X/34.

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13

Thomas, Matthew Robert. "Functional analysis of the ALS/FTD associated gene FUS using a novel in vitro genomic DNA expression system." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:176cbd1b-623e-41cb-9237-cd6c82fc0ad4.

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Aggregations of fused in sarcoma (FUS), a multifunctional RNA processing protein, define a pathological subtype of both frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS), whilst mutations in the FUS gene are causative for ALS. To model the impact of FUS mutations, expression vectors containing the entire genomic sequence of FUS, up and downstream regions, and native promoter sequences have been generated. The constructs have been tagged with an mCherry fluorescent tag, and three separate pathological mutations (R244C, R521C, and P525L) have been separately inserted. Transgenic mice have been generated using the WT and P525L FUS vectors to provide a highly physiological model of FUS in disease. Within transfected HEK293 cells, insertion of the P525L and R521C FUS mutations leads to relocalisation of FUS from the nucleus to the cytoplasm. R521C and P525L mutant FUS incorporates into cytoplasmic aggregations of untranslated mRNA and RNA binding proteins known as stress granules. The strong relocalisation seen with P525L-FUS is associated with a gain of cytotoxicity. Reversal of this cytoplasmic relocalisation by demethylation of FUS rescues this cytotoxicity, suggesting a toxic gain of cytoplasmic function in the majority of FUS mutations. By contrast, insertion of the R244C mutation leads to neither relocalisation, stress granule association, nor cytotoxicity. Notably the R244C mutation, located away from the nuclear localization domain in which the majority of FUS mutations are found, leads to the presence of smaller FUS fragments in western blot analyses. These fragments appear not to be due to splicing defects in FUS but rather are due to post-translational modifications or aberrant protein cleavage. These data suggest an alternative pathway for FUS toxicity based upon a nuclear loss of function.
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Hernández, Ruiz Mª Isabel. "Factores genéticos asociados a la degeneración lobar frontotemporal. Análisis de susceptibilidad genética y correlación fenotipo-genotipo." Doctoral thesis, Universitat Autònoma de Barcelona, 2014. http://hdl.handle.net/10803/285735.

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La Degeneración Lobar Frontotemporal es un grupo heterogéneo de enfermedades, la segunda causa más frecuente de demencia en edad presenil y la que presenta el mayor número de casos hereditarios. Se caracteriza por una gran variabilidad clínica, genética e histopatológica. Las personas afectas pueden presentar síntomas que abarcan desde los trastornos de conducta hasta las diferentes alteraciones del lenguaje, con o sin enfermedad de motoneurona o parkinsonismo asociado. La atrofia en los lóbulos frontales y temporales es el hallazgo radiológico más relevante. En los últimos 10 años, el conocimiento de esta entidad clínica ha presentado remarcables cambios a nivel genético e histopatológico que han servido para establecer criterios clínicos más consistentes. Hasta el momento han sido descritos diez genes asociados a DLFT y cuatro diferentes proteínas de agregación han sido detectadas en los cerebros afectos. Este trabajo aporta la experiencia clínica de más de 15 años en pacientes con DLFT y el trabajo de colaboración con diferentes grupos de investigación en genética de enfermedades neurodegenerativas.
Frontotemporal Lobar Degeneration is a heterogeneous group of disorders, the second most frequent cause of early dementia and the one with the highest number of inherited cases. It is characterized by considerable variability in clinical, genetic and histopathologic features. Patients may present symptoms ranging from behavioural disturbances to different language disorders, with or without motor neuron disorders or associated Parkinsonism. Atrophy in frontal and temporal lobes is the most relevant radiological finding. In the last 10 years, the knowledge of this clinical entity has undergone remarkable changes both genetically and histopathologically, which have served to establish more consistent clinical criteria. Until now 10 genes causative of dementia have been described and up to four different proteins causative of atrophy have been detected in aggregates. This work provides the clinical experience of more than 15 years with DLFT patients and the collaborative work with different Genetic Research Groups in Neurodegenerative Disorders
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Strecker, Katrin [Verfasser], and Christian [Akademischer Betreuer] Haass. "Linking neurodegeneration to vascular dysfunction - Loss of ALS/FTD-associated TDP-43 causes angiogenic defects / Katrin Strecker ; Betreuer: Christian Haass." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2016. http://d-nb.info/1126407437/34.

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Hartmann, Hannelore [Verfasser], and Christian [Akademischer Betreuer] Haass. "The interactomes of ALS/FTD associated poly-GR/PR link protein translation to disease pathogenesis / Hannelore Hartmann ; Betreuer: Christian Haass." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1208150146/34.

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17

Sinigaglia-Amadio, Sabrina Leveratto Jean-Marc. "Une approche sociologique du travail associatif dans les quartiers dits sensibles de l'expérience à l'expertise /." [S.l.] : [s.n.], 2007. ftp://ftp.scd.univ-metz.fr/pub/Theses/2007/Sinigaglia_Amadio.Sabrina.LMZ0709.pdf.

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Heß, Martin [Verfasser], Jens C. [Akademischer Betreuer] Brüning, and Aleksandra [Akademischer Betreuer] Trifunovic. "The fat mass and obesity-associated protein (Fto) regulates activity of the dopaminergic circuitry / Martin Heß. Gutachter: Jens C. Brüning ; Aleksandra Trifunovic." Köln : Universitäts- und Stadtbibliothek Köln, 2014. http://d-nb.info/1050577000/34.

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Hedberg, Lilia. "Identification of obesity-associated SNPs in the human genome : Method development and implementation for SOLiD sequencing data analysis." Thesis, Linköpings universitet, Institutionen för klinisk och experimentell medicin, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-57932.

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Over the last few years, genome-wide association studies (GWAS) have been used to identify numerous obesity associated SNPs in the human genome. By using linkage studies, candidate obesity genes have been identified. When SNPs in the first intron of FTO were found to be associated to BMI, it became the first gene to be linked to common obesity. In order to look for causative explanations behind the associated SNPs, a re-sequencing of FTO had been performed on the SOLiD sequencing platform. In-house candidate gene, SLCX, was also sequenced in order to evaluate a potential obesity association. The purpose of this project was to analyse the sequences and also to evaluate the quality of the SOLiD sequencing. A part of the project consisted in performing PCRs and selecting genomic regions for future sequencing projects. I developed and implemented a sequence analysis strategy to identify obesity associated SNPs. I found 39 obesity-linked SNPs in FTO, a majority of which were located in introns 1 and 8. I also identified 3 associated intronic SNPs in SLCX. I found that the SOLiD sequencing coverage varies between non-repetitive and repetitive genomic regions, and that it is highest near amplicon ends. Interestingly, coverage varies significantly between different amplicons even after repetitive sequences have been removed, which indicates that it is affected by features inherent to the sequence. Still, the observed allele frequencies for known SNPs were highly correlated with the SNP frequencies documented in HapMap. In conclusion, I verify that SNPs in FTO are associated with obesity and also identify a previously unassociated gene, SLCX, as a potential obesity gene. Re-sequencing of genomic regions on the SOLiD platform was proven to be successful for SNP identification, although the difference in sequencing coverage might be problematic.
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Berulava, Tea [Verfasser], Bernhard [Akademischer Betreuer] Horsthemke, Anke [Akademischer Betreuer] Hinney, and Ulrich [Akademischer Betreuer] Rüther. "Expression and function of the fat mass and obesity-associated gene FTO / Tea Berulava. Gutachter: Bernhard Horsthemke ; Anke Hinney ; Ulrich Rüther. Betreuer: Bernhard Horsthemke." Duisburg, 2013. http://d-nb.info/1035066386/34.

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Ramos, Ramon Bossardi. "Gene ligado a obesidade e massa gorda (fat mass and obesity associated; fto), menopausa e fatores de risco cardiovascular em mulheres na pós-menopausa." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2011. http://hdl.handle.net/10183/30937.

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Obesidade é uma doença crônica multifatorial que no Brasil atinge cerca de 12,4% dos homens e 16,9% das mulheres com mais de 20 anos. No período pós menopáusico, as mulheres apresentam uma série de alterações fisiológicas, entre elas alteração na distribuição de gordura corporal, sobretudo um aumento na região abdominal. A obesidade apresenta uma etiologia poligênica e diversos genes vêm sendo estudados, entre eles o gene ligado a obesidade e massa gorda (FTO) que já se mostrou fortemente associado com a obesidade/IMC. Mas em relação a parâmetros metabólicos e marcadores de risco cardiovascular, os estudos ainda são bastante controversos dependendo da população em estudo. Com esses dados nosso trabalho buscou a associação entre os polimorfismos rs9939609 e rs8050136 do gene FTO com variáveis metabólicas e de risco cardiovascular em mulheres na pós menopausa. Nosso estudo mostrou que no SNP rs9939609, o genótipo homozigoto para o alelo A está associado com aumento da relação cintura quadril, índice de acumulação lipídica (LAP), que é um marcador de risco cardiovascular, que é um marcador de risco cardiovascular e hipertensão. Enquanto que no SNP rs8050136, o genótipo em homozigose para o alelo A foi associado com pressão arterial diastólica e LAP. Tanto o genótipo polimórfico do SNP rs9939609 e selvagem do rs8050136 foram associados com alteração nos níveis de glicose plasmática. Deste modo, podemos concluir que o polimorfismo rs9939609 no gene do FTO pode ser um preditor de maior risco cardiovascular em mulheres na menopausa.
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Dietrich, Kerstin [Verfasser], Peter [Akademischer Betreuer] Kovacs, Michael [Akademischer Betreuer] Stumvoll, and Unbekannt [Gutachter] Unbekannt. "Molekulare Evolution der metabolisch relevanten Gene MTNR1B (Melatoninrezeptor 1B) und FTO (Fat Mass and Obesity Associated) / Kerstin Dietrich ; Gutachter: Unbekannt Unbekannt ; Peter Kovacs, Michael Stumvoll." Leipzig : Universitätsbibliothek Leipzig, 2013. http://d-nb.info/1238242472/34.

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Horvath, Jaqueline Driemeyer Correia. "Genética da obesidade : polimorfismos do LEPR (rs1137101 e rs8179183), FTO (rs9939609) e suas associações com transtorno alimentar e parâmetros nutricionais em pacientes obesos." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2017. http://hdl.handle.net/10183/164918.

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Percy, Linda Ann. "An investigation of the phytoplankton of the Fal Estuary, UK and the relationship between the occurrence of potentially toxic species and associated algal toxins in shellfish." Thesis, University of Westminster, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.434277.

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Sarter, Michael [Verfasser], Payam [Gutachter] Akhyari, and Thomas [Gutachter] Höhn. "Einfluss des Fto-Gens (fat mass and obesity-associated gene) auf degenerative Prozesse in bovinem Glutaraldehyd-fixiertem Herzklappen-Bioprothesenmaterial in einem Knockout-Mausmodell / Michael Sarter ; Gutachter: Payam Akhyari, Thomas Höhn." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2020. http://d-nb.info/1205969470/34.

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26

Scarlato, Michele. "Sicurezza di rete, analisi del traffico e monitoraggio." Master's thesis, Alma Mater Studiorum - Università di Bologna, 2012. http://amslaurea.unibo.it/3223/.

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Il lavoro è stato suddiviso in tre macro-aree. Una prima riguardante un'analisi teorica di come funzionano le intrusioni, di quali software vengono utilizzati per compierle, e di come proteggersi (usando i dispositivi che in termine generico si possono riconoscere come i firewall). Una seconda macro-area che analizza un'intrusione avvenuta dall'esterno verso dei server sensibili di una rete LAN. Questa analisi viene condotta sui file catturati dalle due interfacce di rete configurate in modalità promiscua su una sonda presente nella LAN. Le interfacce sono due per potersi interfacciare a due segmenti di LAN aventi due maschere di sotto-rete differenti. L'attacco viene analizzato mediante vari software. Si può infatti definire una terza parte del lavoro, la parte dove vengono analizzati i file catturati dalle due interfacce con i software che prima si occupano di analizzare i dati di contenuto completo, come Wireshark, poi dei software che si occupano di analizzare i dati di sessione che sono stati trattati con Argus, e infine i dati di tipo statistico che sono stati trattati con Ntop. Il penultimo capitolo, quello prima delle conclusioni, invece tratta l'installazione di Nagios, e la sua configurazione per il monitoraggio attraverso plugin dello spazio di disco rimanente su una macchina agent remota, e sui servizi MySql e DNS. Ovviamente Nagios può essere configurato per monitorare ogni tipo di servizio offerto sulla rete.
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Silva, Rita Sofia Bettencourt. "TSH, FT3 and FT4 were not associated with changes in body composition in HIV-infected patients on combined antiretroviral therapy." Dissertação, 2012. https://repositorio-aberto.up.pt/handle/10216/72343.

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Silva, Rita Sofia Bettencourt. "TSH, FT3 and FT4 were not associated with changes in body composition in HIV-infected patients on combined antiretroviral therapy." Master's thesis, 2012. https://repositorio-aberto.up.pt/handle/10216/72343.

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Tsai, Yueh-Lin. "Function and Regulation of ALS/FTD-associated RNA Binding Protein FUS." Thesis, 2021. https://doi.org/10.7916/d8-j4g9-m045.

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Fused in Sarcoma (FUS) is a nuclear RNA binding protein functioning in a number of essential cellular processes such as RNA processing and DNA damage response. Mutations in FUS gene contribute to 5% of familial Amyotrophic Lateral Sclerosis (ALS) characterized by FUS protein cytoplasmic aggregation. Despite efforts have been made in the past decade, mechanisms of FUS aggregates to induce cytotoxicity are not fully understood. In addition, wild-type FUS protein has been found mis-localized to cytoplasm in sporadic ALS and Frontotemporal Dementia (FTD) patients with unclear mechanisms. Here, we aimed to address the functional consequences of ALS mutant FUS aggregation and investigate the mechanisms of wild-type FUS cytoplasmic translocation. This dissertation is divided into three parts: In the first part, we review pathophysiological mechanisms of FUS and other ALS mutant genes which induce cell death via disrupting six major cellular processes: mRNA processing, non-sense mediated decay, mitochondrial functions, nucleocytoplasmic transport, autophagy and DNA damage response. In the second part, we aimed to understand the functional consequences of RNA sequestration by FUS aggregates. We performed RNA immunoprecipitation against exogenous or endogenous FUS in the transfected cell lines and mutant FUS ALS patient fibroblasts to isolate RNAs associated with wild-type or ALS mutant FUS. Next, we analyzed the isolated RNAs using poly(A+) RNA-specific sequencing 3’READS and RT-qPCR, and we found many nuclear-encoded respiratory chain complex mRNAs are top-enriched transcripts associated with ALS mutant or overexpressed wild-type FUS. We further demonstrated that respiratory chain complex mRNAs are sequestered in mutant FUS cytoplasmic aggregates and the encoded protein expression levels are suppressed. Finally, we showed that knockdown of respiratory chain complex proteins encoded by FUS-sequestered transcripts can recapitulate mitochondrial dysfunction observed in FUS-transfected cell lines. Our findings in the second part thus provides a novel mechanism by which ALS mutant FUS, as well as overexpressed wild-type FUS, to induce mitochondrial dysfunction via preferential sequestration of respiratory chain complex mRNAs. The third part focuses on understanding pathways affecting FUS nucleocytoplasmic distribution. By using pharmacological treatments and immunofluorescence, we found that nuclear RNA transcription, export and decay substantially modulate nucleocytoplasmic distribution of wild-type FUS protein. Moreover, we report that FUS antibodies used in immunofluorescence significantly affect the results of nucleocytoplasmic ratio quantification. Intriguingly, we observed altered serine-2/-5 phosphorylation on RNAPII CTD as well as reduced number of nascent transcripts in sporadic ALS patient cells, indicating aberrant transcriptional activity related to cytoplasmic accumulation of nuclear RNA binding proteins. Our findings in the third part provide insights to the importance of nuclear RNA metabolism in modulating FUS localization. We also addressed the inconsistent results reported in previous studies regarding FUS nucleocytoplasmic distribution in response to stress. Altogether, these findings suggest proof-of-principle mechanisms of FUS toxic function and aberrant localization linked to ALS and FTD disease spectrum.
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藤岡, 祐介, and Yusuke Fujioka. "FUS-regulated region- and cell-type-specific transcriptome is associated with cell selectivity in ALS/FTLD." Thesis, 2013. http://hdl.handle.net/2237/19158.

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Dietrich, Kerstin. "Molekulare Evolution der metabolisch relevanten Gene MTNR1B (Melatoninrezeptor 1B) und FTO (Fat Mass and Obesity Associated)." Doctoral thesis, 2011. https://ul.qucosa.de/id/qucosa%3A11832.

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Die hier vorliegende Arbeit zeigt die molekulare Evolution des Melatoninrezeptor 1 B-Gens (MTNR1B) und des Fat Mass and Obesity Associated-Gens (FTO). Für beide Gene wurden in genomweiten Assoziationsstudien (GWAS) Varianten entdeckt, welche zu der Entwicklung einer Adipositas bzw. deren Folgeerkrankungen beitragen können. So wurde für Einzelbasenaustausche (SNPs) im MTNR1B (rs10830963, rs4753426) eine Verschlechterung der Nüchternglukose sowie der Insulinausschüttung gezeigt. Zudem wurde für die Allelfrequenz des rs4753426 C-Allels ein Zusammenhang mit der täglichen Sonnenscheindauer beschrieben. Im FTO wurde eine (tagging) Variante im ersten Intron identifiziert (rs9939609), welche einen erhöhten Körpermasseindex (BMI) zu vermitteln scheint und robust repliziert werden konnte. Zusätzlich konnte in den Sorben, einer in der Lausitz ansässigen Volksgruppe, eine Variante im dritten Intron (rs17818902) beschrieben werden, die ein zusätzliches, stärkeres Assoziationssignal mit einem erhöhten BMI zeigte. Dies führte zu der Fragestellung, ob MTNR1B und FTO einer Konservierung unterlegen sind. Zudem interessierten populationsspezifische Unterschiede, um die Untersuchungen in den Kontext der Hypothese des sparsamen Genotyps stellen zu können. Demnach haben Individuen mit einer genetischen Veranlagung, die ihnen eine effizientere Energiespeicherung ermöglicht, zu Zeiten von Nahrungsmangel einen Fitness-Vorteil gegenüber Nicht-Trägern. Die Konservierung zwischen den Spezies wurde mit Phylogenetic Analysis by Maximum Likelihood (PAML) betrachtet, eine Analyse die auf dem Verhältnis von nichtsynonymen zu synonymen Basenaustauschen innerhalb einer kodierenden Sequenz beruht. Die Selektion innerhalb bzw. zwischen menschlichen Populationen wurde anhand verschiedener populationsgenetischer Variablen näher beleuchtet. Sowohl für MTNR1B als auch für FTO konnte gezeigt werden, dass sie über die betrachteten Spezies im Durchschnitt stark oder sehr stark konserviert sind, was die physiologische Relevanz dieser Gene untermauert. Für MTNR1B zeigte sich zudem, dass es auf dem Ast zum Menschen nicht konserviert, sondern positiv selektioniert ist. Dies kann als Anzeichen für durch die Umwelt bedingte Einflüsse gedeutet werden. Essentielle Residuen des Rezeptors sind jedoch auch hier hochgradig konserviert. Die populationsgenetischen Variablen implizieren bei beiden Genen eine nicht-neutrale Selektion. Während sich beim MTNR1B insbesondere populationsspezifische Unterschiede anhand des Fixierungsindex Fst zeigten, konnten für FTO marginal signifikante Korrelationen zwischen der Konservierung der Haplotypen und der Stärke der Assoziation mit BMI in den Sorben gezeigt werden. Für beide Gene kann die Hypothese des sparsamen Genotyps nicht prinzipiell ausgeschlossen werden, allerdings sind weitere Untersuchungen diesbezüglich von Nöten.
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Wang, Ling-Yi, and 王齡儀. "SNP Genotypes of PNAS-4, CSTF1, ACTA2, APOM, IRS-1 and FTO Genes Associated with Major Performances in Pigs." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/81234780748315415411.

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Gill, Richard. "Genetic Epidemiological Characterization of Two Major Obesity Candidate Genes: The 16p11.2 BP4-BP5 Microdeletion and the Fat-Mass and Obesity-Associated (FTO) Locus." Thesis, 2016. https://doi.org/10.7916/D8D79B5Z.

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Background: The obesity epidemic is the greatest public health problem of our time, and exerts an enormous health and economic burden by acting as a risk factor for multiple disorders and all-cause mortality. While environmental and social factors certainly contribute to the complex etiology of obesity, there is strong evidence of a substantial genetic component. The majority of obesity genes are involved the leptin-melanocortin receptor pathway governing energy homeostasis, but mutations affecting this circuit are often untreatable and rare, and an improved understanding of other genetic risk factors could aid in the development of novel therapies. In this thesis I study two obesity candidate genes with unclear direct relevance to disease: 1) rare structural variation at the 16p11.2 BP4-BP5 locus and 2) common variation in the Fat Mass and Obesity-Associated (FTO) gene. Methods: 1) I analyzed disinhibited eating measurements from families with 16p11.2 copy number variation (CNV) carriers, to test whether eating in the absence of hunger (EAH) and loss of control (LOC) eating behaviors mediate the dosage-dependent CNV-BMI relationship. 2) Using association data from a study of over 20,000 African Americans and 1,145 functional annotations from the Encyclopedia of Non-coding Elements (ENCODE) and Roadmap Epigenomics projects, I statistically fine-mapped the FTO locus to identify the SNP(s) and cellular contexts underlying the association between FTO and obesity. Results: 1) EAH due to external triggers mediates over 30% of the 16p11.2 deletion’s effect on obesity, while other EAH and LOC behaviors were not significant mediators. This result was independent of IQ deficits and autism related to the CNV, as well as parents’ feeding behaviors and practices. 2) Given 51 FTO SNPs’ association statistics, correlation, and overlap with functional annotations, rs9927317 and rs62033405 had the highest posterior probability of association with obesity. Obesity-associated SNPs may regulate expression of FTO and/or nearby genes through the activity of enhancers and 5’ ends of transcribed genes in the substantia nigra of the brain, bone chondrocytes, and white adipose. Conclusions: These results may help pinpoint the specific genes, regulatory elements, and cellular contexts through which the 16p11.2 and FTO loci exert their effects on obesity.
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Poritsanos, Nicole Joanna. "Nutritional regulation of central fat mass and obesity-associated (FTO) expression, and its association with the central melanocortin signaling in the regulation of energy homeostasis." 2010. http://hdl.handle.net/1993/4294.

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The central nervous system (CNS) melanocortin signaling pathway plays a critical role in the regulation of metabolism. However, the regulatory effects of CNS melanocortin signaling on hepatic lipid metabolism and fatty liver disease have not been well established. Although the activity of the CNS melanocortin system is regulated by metabolic signals, the mechanism for this regulation is not fully understood. Variants of the FTO (fat mass and obesity-associated) gene are associated with obesity and FTO is expressed in the hypothalamic neurons including proopiomelanocortin (POMC) neurons. Therefore, it is hypothesized that hypothalamic FTO plays a role in the regulation of metabolism by mediating the effect of metabolic signals on hypothalamic melanocortinergic neurons, and that impairments in this regulation may cause metabolic impairments including obesity and fatty liver disease. Intracerebroventricular (i.c.v.) treatment with SHU9119, a melanocortin antagonist, increased hepatic lipid accumulation and the expression of genes encoding lipogenic enzymes in lean mice. Conversely, i.c.v. treatment with MTII, a melanocortin agonist, reduced the expression of hepatic lipogenic genes in association with reduction in body weight in ob/ob mice, a mouse model of fatty liver disease. Immunohistochemical analysis demonstrated that Fto is co-expressed in both POMC and agouti-related protein (AgRP) neurons in the mouse hypothalamus. Fto mRNA and protein expression was reduced by fasting and increased by glucose treatment in nutritionally important hypothalamic nuclei. Fasting-induced reduction in hypothalamic Fto expression was observed in both lean wild-type and obese ob/ob mice, while the stimulatory effect of glucose on hypothalamic Fto expression was absent in ob/ob mice. These findings support the hypothesis that central melanocortin signaling regulates hepatic lipid metabolism in part by regulating de novo lipogenesis. Impairments in the central melanocortin signaling lead to the development of hepatic steatosis, while enhanced melanocortin signaling may be beneficial in reversing abnormal hepatic lipid metabolism in fatty liver disease (Poritsanos et al., 2008). These findings also support the hypothesis that Fto is expressed in the hypothalamic melanocortinergic neurons and is regulated by metabolic signals involving changes in CNS glucose availability and/or glucose action. Impairments in this regulation may cause metabolic impairments including obesity and fatty liver disease.
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Perozo-Marin, Francisco Antonio. "Investigations on avian adeno-associated virus based protein expression for poultry vaccination, the VG/GA strain of Newcastle disease virus (NDV) and the use of FTA cards for NDV detection." 2008. http://purl.galileo.usg.edu/uga%5Fetd/perozo%5Ffrancisco%5Fa%5F200805%5Fphd.

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36

Tsai, Pei-Ting, and 蔡佩廷. "Association Studies of Genetic Polymorphisms in the Human SA Gene (SAH) and Fat Mass and Obesity Associated (FTO) Gene and Cardiometabolic Risk Factors: the Stanford Asian-Pacific Program of Hypertension and Insulin Resistance (SAPPHIRe) Study." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/03752114431931217651.

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碩士
國立陽明大學
公共衛生研究所
99
Objectives The risk factors of cardiometabolic syndrome include hypertension, hyperglycemia, dyslipidemia, and obesity. SAH gene is a candidate gene that is associated with hypertension while FTO gene is associated with obesity. The objective of this study is to investigate the association between SAH and FTO polymorphisms and cardiometabolic risk factors in SAPPHIRe study. Methods The study was a part of Stanford Asian-Pacific Program of Hypertension and Insulin Resistance (SAPPHIRe), a sibling-based study. We included 894 Chinese subjects with DNA sample available. Genotyping of SAH polymorphisms (rs55810929, rs11647477 and rs5716) and FTO polymorphisms (rs1421085, rs9939609 and rs9939506) were performed using the TaqMan Assay. Results In our study, we found significant association between SAH rs55810929 allele type and triglycerides levels. We also observed significant association between rs1164747 and rs5716 polymorphisms of SAH gene and hypertension as well as fasting plasma glucose levels. The rs11647477 was found be to significantly associated with HOMA-IR and the rs5716 was found to be significantly associated with non-high density lipoprotein level. We further found significant difference in haplotype frequencies between hypertension and non-hypertension groups. Those subjects carrying rs11647477 and rs5716 GG haplotype have decreased risk of hypertension. There were significant difference in the genotype distributions of rs1421085 and rs9930506 polymorphisms of FTO gene between hypertension and non-hypertension group as well as top and bottom of one-third of triglycerides level. We also found significant association between the allele type distribution of rs9930506 and high-density lipoprotein level as well as HOMA-IR. Conclusions In the present study, we found the SAH polymorphisms are associated with hypertension, higher triglycerides levels, higher plasma glucose, higher non-high density lipoprotein and higher HOMA-IR. We also found FTO polymorphisms are associated with hypertension, triglycerides level, high-density lipoprotein level and HOMA-IR.
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