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1
Corcoran, Cecily. „GENIUS LOCI“. VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/2655.
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I attempt to capture the simple and fleeting beauty of Washington, DC, before it folds into time. In my representational paintings and monotypes, I want to convey the elegance and serenity of the streets, cars, pedestrians, and the majestic buildings of our nation’s capital. As a native Washingtonian, I’ve always admired the view of the city from across the Potomac River, from sunrise to sunset. I want to share these views and these experiences of my daily life with the viewer.
2
Kudělka, Vladimír. „Genius loci“. Master's thesis, Vysoké učení technické v Brně. Fakulta výtvarných umění, 2013. http://www.nusl.cz/ntk/nusl-232388.
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3
Zhao, Yuxuan. „Genius Loci---Vertical Temple Design“. Thesis, Virginia Tech, 2019. http://hdl.handle.net/10919/87756.
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China is a high speed developing country during the past 40 years. However, when China became better and better, there were a lot of issues being left, such as boomed populations, urban village emerging, social media issues and lack of human spirit. All of these issues occurred in the modern urban context, which made the "Loci Genius" lose.
So how could architects reconstruct and conserve the "Genius Loci." I try to build the temple for people in the high dense city, which help people to find and think for themselves, to keep peaceful. I believe people and space could build the journey to the pilgrimage. The Buddha joss will not be made in the temple, but be established in every visitor's mind finally.M. Arch.
4
Nyström, Per-Erik. „Quantitative trait loci in pig production /“. Uppsala : Swedish Univ. of Agricultural Sciences (Sveriges lantbruksuniv.), 1999. http://epsilon.slu.se/avh/1999/91-576-5712-2.pdf.
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5
Chan, Lai-kuen Jenny, und 陳麗娟. „Genius Loci: Tin Hau Temple, Aberdeen“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31985051.
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6
Aba'a, Megne Harry. „Lex loci protectionis et droit d'auteur“. Thesis, Université Côte d'Azur, 2020. http://theses.univ-cotedazur.fr/2020COAZ0013.
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Le principe de territorialité domine la matière de la propriété intellectuelle et en particulier celle du droit d’auteur. Si ce principe et la règle de conflit qu’il inspire, la lex loci protectionis, constituaient de véritables avancées à la fin du XIXème s., de nos jours, ils peinent à convaincre. En effet, le principe de territorialité qui est rattachable au principe de souveraineté dans sa dimension de régulation de l’ordre juridique interne subit de multiples remises en cause. Or, en raison de l’intensification des échanges transnationaux, de l’extension des marchés, de la montée des pouvoirs privés économiques, de l’exploitation dématérialisée des œuvres et notamment, la possibilité de les diffuser sur des réseaux mondiaux comme internet, la souveraineté tend à perdre en puissance. Cela oblige à questionner la pertinence d’un rattachement territorial vis-à-vis de réalités a-territoriales. Le maintien tel quel du principe de territorialité, en termes de conflit de lois, atteint alors la sécurité juridique et les attentes légitimes des parties. Le parti pris de ces travaux est celui d’une réévaluation. Il ressort en effet que le recul dans les relations transnationales du principe de souveraineté - qui sous-tend le principe de territorialité - devrait se traduire sur le plan de la règle de conflit, par un recul de ladite territorialité. A rebours de la tendance générale qui consacre l’hégémonie de la lex loci protectionis, les présents travaux proposent d’une part, d’en circonscrire la compétence dans les domaines où le principe de territorialité ne s’impose pas comme une nécessité, et d’autre part de réorienter le rattachement de manière à limiter la concurrence des lois applicables. Il s’agit, en d’autres termes, de réserver une place à l’universalisme compris comme un rempart contre la variabilité du droit applicable et l’insécurité juridique que cette variabilité pourrait emporterThe principle of territoriality dominates the field of intellectual property and that of copyright. If this principle and the conflict rule it inspires, the lex loci protectionis, were real advances at the end of the 19th century, they are nowadays difficult to convince. Indeed, the principle of territoriality, which is linked to the principle of sovereignty in its dimension of regulation of the internal legal order, is undergoing multiple challenges. However, because of the intensification of transnational exchanges, the extension of markets, the rise of private economic powers, the dematerialised exploitation of works and in particular the possibility of disseminating them on global networks such as the Internet, sovereignty tends to lose significance. This forces us to question the relevance of a territorial connection to a-territorial realities. Maintaining the principle of territoriality as it stands, in terms of conflict of laws, then reaches legal security and the legitimate expectations of the parties. The approach taken in this work is that of a re-evaluation. It emerges in fact that the retreat in transnational relations of the principle of sovereignty - which underlies the principle of territoriality - should be translated in terms of conflict rule by a retreat of the said territoriality. Against the general trend which confirms the hegemony of the lex loci protectionis, the present work proposes, on the one hand, to circumscribe its competence in the fields where the principle of territoriality is not imposed as a necessity, and on the other hand to reorient the connection in such a way as to limit the competition of the applicable laws. In other words, to reserve a place for universalism understood as a bulwark against the variability of the applicable law and the legal insecurity that this variability could entail
7
Turri, Maria Grazia. „Mapping of behavioural quantitative trait loci“. Thesis, University of Oxford, 2002. http://ora.ox.ac.uk/objects/uuid:89823fa1-c1d3-49e3-acb9-46da18b12245.
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Anxiety is a common disorder which affects about 25% of the population and whose pathophysiology is still poorly understood. Animal models of disease have been widely used to investigate the molecular basis of human disorders, including psychiatric illnesses. This thesis is about the study of the genetic basis of a mouse model of anxiety. I have carried out a QTL mapping study of behavioural measures thought to model anxiety. I report results from 1,636 mice, assessed for a large number of phenotypes in five ethological tests. Mice belonged to two F2 intercrosses originated by four lines generated in a replicate selection experiment. By comparing mapping results between the two crosses, I have demonstrated that selection operated on the same relatively small number of loci in the four selected lines. Analysis of genetic effect of QTL across phenotypes has allowed me to identify loci with specific roles on different dimensions of anxious behaviour, therefore enhancing our understanding of the anxiety phenotype in mice. For some of these QTL I have also accomplished fine mapping experiments: a locus on chromosome 15 is now contained in an interval of only 3 centimorgans. This work is the basis for further molecular dissection of the genetic loci that underlie anxiety and provides a starting point for the discovery of genes involved in a common psychiatric condition.
8
Raine, Emma Victoria Angela. „Expression analysis of osteoarthritis susceptibility loci“. Thesis, University of Newcastle upon Tyne, 2014. http://hdl.handle.net/10443/2753.
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Osteoarthritis (OA) is a common disease characterised by the progressive loss of the articular cartilage of synovial joints. It is multifactorial and polygenic. Candidate genebased association studies and genome-wide association scans (GWAS) have been used to identify OA risk alleles with over 10 regions of the human genome so far reported as harbouring OA susceptibility. Expression quantitative trait loci (eQTLs) demonstrate a correlation between gene expression levels and DNA polymorphism, the assumption being that the polymorphism resides within a regulatory element of the gene. The functional polymorphism can be cis-acting (within or close to the gene) or trans-acting (located a distance from the gene). It has become apparent for many common diseases that the majority of risk alleles are eQTLs rather than polymorphisms that alter amino acid sequences. The aim of this thesis was to investigate whether genes proximal to or harbouring OA-associated polymorphisms identified by GWAS are subject to cisregulation, which could therefore be contributing to the association signal. The expression levels of the genes were analysed in joint tissues from OA patients who had undergone joint replacement. Overall gene expression was measured by quantitative PCR whilst allelic expression was assessed using assays that can distinguish mRNA output from each allele of a transcript SNP. The functional effect of SNPs was tested in vitro using luciferase reporter assays. Expression analysis of genes at the OA-associated chromosome 7q22 locus identified HBP1 as the likely target of the OA susceptibility mapping to this region. Expression analysis of SMAD3 and GNL3 identified eQTLs active in OA joint tissues for both genes, whilst luciferase reporter assays identified two 3´UTR SNPs as potential mediators of the SMAD3 eQTL. Overall, this thesis demonstrates that OA tissues are subject to a range of regulatory elements that can influence disease during development or ageing.
9
George, Thomas. „A distributed memory implementation of Loci“. Master's thesis, Mississippi State : Mississippi State University, 2001. http://library.msstate.edu/etd/show.asp?etd=etd-11082001-140719.
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10
Chan, Lai-kuen Jenny. „Genius Loci : Tin Hau Temple, Aberdeen /“. Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B25947539.
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11
Peticca, Marcella. „Genuis loci: Perdita e riscoperta del luogo“. Master's thesis, Alma Mater Studiorum - Università di Bologna, 2015. http://amslaurea.unibo.it/9702/.
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Il Genius Loci, affrontato nelle sue caratteristiche e analizzato tra la perdita e la riscoperta del luogo, è il filo conduttore per la rilettura di un percorso, che si snoda attraverso le esperienze didattiche progettuali maturate durante il corso di studi.
L’analisi del concetto di luogo avviene secondo la lettura data dagli architetti che in particolare ne hanno promosso il confronto, Aldo Rossi e Christian Norberg-Schulz, nella loro interpretazione volta alla riscoperta della memoria del luogo e dell’identificazione con esso.
Se da una parte c’è una valutazione della sedimentazione storica, individuata come memoria imprescindibile; dall’altra c’è un apprezzamento delle caratteristiche intrinseche del sito, che ne costituiscono la sua identità.
Il confronto con alcuni scritti di Umberto Cao e Franco Purini ha permesso di concludere un lungo discorso, riallacciandolo al dibattito culturale che aveva suscitato.
Per avvicinarci a questo concetto di rispetto del luogo e alla sua valorizzazione si sono presentati due progetti, che ne rappresentano da una parte la piena realizzazione e dall’altra il fallimento e questi sono il Centro culturale Jean-Marie Tjibaou a Nouméa in Nuova Caledonia di Renzo Piano ed il progetto Nexus di un complesso di abitazioni a Fukuoka, in Giappone, coordinato da Arata Isozaky.
I progetti maturati durante le esperienze didattiche e presentati per un confronto sul tema sono: Un giardino in forma di teatro, progettato per il quadrilatero di Cervia, con la professoressa Maura Savini; Tre edifici per uffici e pubblici esercizi, realizzati all’interno di un intervento di gruppo più ampio, sulla Vena Mazzarini, a Cesenatico, affrontati con il professor Jose’ Charters Monteiro; un Edificio per il rilevamento delle acque, in prossimità di Kleve, in Germania, realizzato durante il periodo Erasmus, svoltosi presso la Fachhochschule di Colonia, con il professor Hannes Hermanns.
12
Santana, Morant Dámaris. „Bayesian mapping of multiple quantitative trait loci“. [Gainesville, Fla.] : University of Florida, 2005. http://purl.fcla.edu/fcla/etd/UFE0012166.
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13
Mcgovern, Amanda Jane. „Functional characterisation of rheumatoid arthritis risk loci“. Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/functional-characterisation-of-rheumatoid-arthritis-risk-loci(9c2cfbf0-3a1e-424f-942e-a58b108b7b94).html.
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Rheumatoid arthritis (RA) is a complex autoimmune disease affecting approximately 1% of the population. Multiple factors contribute to the development of RA, with genetic factors accounting for around 60% of the disease risk. Over the last few years, genome-wide association studies (GWAS) have successfully been used to identify regions of the genome predisposing to complex disease. There are now 101 confirmed RA risk loci, but for the vast majority of these loci the causal gene and causal variant remain unidentified and therefore, their function in disease is unexplored. The majority of genetic variants, or single nucleotide polymorphisms (SNPs), associated with disease map to non-coding enhancer regions, which may regulate transcription through long-range interactions with their target genes. The aims of this project were to identify the causal genes within an RA locus, pinpoint the causal variants and elucidate the mechanisms by which the variants modify gene function. Capture Hi-C (CHi-C) was carried out with the aim of identifying long range interactions between disease-associated SNPs and genes in four related autoimmune diseases. Many long-range interactions were identified which implicated novel candidate genes, interactions involving multiple genetic loci which had a common target, and interactions with loci which had previously been implicated in disease. Complex interaction patterns were observed in many of the disease associated loci, particularly in the 6q23 locus which is associated with a number of autoimmune diseases and is the focus of the present thesis. Within the 6q23 locus, associated SNPs lie a large distance from any gene (>180kb) making it difficult to pinpoint the exact causal gene. Results from CHi-C and chromosome conformation capture (3C-qPCR) experiments indicated that restriction fragments containing disease associated intergenic SNPs could display genotype-specific interactions with genes associated with autoimmunity (IL20RA and IFNGR1). Interactions could also be detected with long non-coding RNAs (lncRNAs), The lead SNP in the 6q23 region is in tight LD with eight other SNPs which are equally likely to be causal. Bioinformatics analysis suggested that the most plausible causal SNP in the 6q23 intergenic region was rs6927172, as it maps to an enhancer in both B-cells and T-cells, is in a DNaseI hypersensitivity cluster, shows transcription factor binding and is in a conserved region. Chromatin immunoprecipitation (ChIP) demonstrated binding of chromatin marks of active enhancers (H3K4me1 and H3K27ac) and the transcription factors BCL3 and NF-κB to the rs6927172 SNP target site in Jurkat T-cells and GM12878 B-cells, suggesting the risk allele could be associated with increased regulatory activity. In conclusion, these results show that CHi-C can help identify novel GWAS causal genes with the potential to suggest novel therapeutic targets. For example IL20RA is already a target for a monoclonal antibody which has been shown to be effective in treating RA in clinical trials. This project has also provided compelling evidence that the autoimmune risk variant in the 6q23 locus, rs6927172, is within a complex gene regulatory region, involving multiple immune genes and regulatory elements, such as lncRNAs.
14
Good, David Andrew, und n/a. „Genetic Loci for Paget's Disease of Bone“. Griffith University. School of Biomolecular and Biomedical Science, 2003. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20040319.125358.
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Paget's disease of the bone is a skeletal disorder of unknown cause. This disease is characterised by excessive and abnormal bone remodelling brought about by increased bone resorption followed by disorganised bone formation. Increased bone turnover results in a disorganised mosaic of woven and lamellar bone at affected skeletal sites. This produces bone that is expanded in size, less compact, more vascular, and more susceptible to deformity or fracture than normal bone. Symptoms of Paget's disease may include bone pain, bone deformity, excessive warmth over bone from hypervascularity, secondary arthritis, and a variety of neurologic complications caused in most instances by compression of the neural tissues adjacent to pagetic bone. Genetic factors play a role in the pathogenesis of Paget's disease but the molecular basis remains largely unknown. The identification of the molecular basis of Paget's disease is fundamental for an understanding of the cause of the disease, for identifying subjects at risk at a preclinical stage, and for the development of more effective preventive and therapeutic strategies for the management of the condition. With this in mind, the aim of this project is to identify genetic loci, in a large pedigree, that may harbour genes responsible for Paget's disease of bone. A large Australian family with evidence of Paget's disease was recruited for these studies (Chapter 3). This pedigree has characterised over 250 individuals, with 49 informative individuals affected with Paget's disease of bone, 31 of whom are available for genotypic analysis. The pattern of disease in these individuals is polystotic, with sites of involvement including the spine, pelvis, skull and femur. Although the affected individuals have a severe early-onset form of the disease, the clinical features of the pedigree suggest that the affected family members have Paget's disease and not familial expansile osteolysis (a disease with some similarities to Paget's disease), as our patients have extensive skull and axial skeletal involvement. The disease is inherited as an autosomal dominant trait in the pedigree with high penetrance by the sixth decade. Due to the large size of this family and multiple affected members, this pedigree is a unique resource for the detection of the susceptibility gene in Paget's disease. The first susceptibility loci for Paget's disease of bone have been mapped by other investigators to chromosome 6p21 (PDB1) and 18q21.1-q22 (PDB2) in different pedigrees. Linkage analysis of the Australian pedigree in these studies was performed with markers at PDB1: these data showed significant exclusion of linkage, with LOD scores < - 2 in this region (Chapter 4). Linkage analysis of microsatellite markers from the PDB2 region excluded linkage with this region also, with a 30 cM exclusion region (LOD score < -2.0) centred on D18S42 (Chapter 4). This locus on chromosome 18q21.1-q22 contains a serine protease (serpin) cluster with similarities to chromosome 6p21. Linkage analysis of this region also failed to provide evidence of linkage to this locus (Chapter 4). These data are consistent with genetic heterogeneity of Paget's disease of bone. A gene essential for osteoclast formation encoding receptor activator of nuclear factor-kB (RANK), TNFRSF11A, has been previously mapped to the PDB2 region. Mutations in the TNFRSF11A gene have been identified segregating in pedigrees with Familial Expansile Osteolysis and early onset familial Paget's disease, however, linkage studies and mutation screening have excluded the involvement of RANK in the majority of Paget's disease patients. For the Australian pedigree, mutation screening at the TNFRSF11A locus revealed no mutations segregating with affected individuals with Paget's disease (Chapter 4). Based on these findings, our hypothesis is that a novel susceptibility gene relevant to the pathogenesis of Paget's disease of bone lies elsewhere in the genome in the affected members of this pedigree; this gene should be identifiable using a microsatellite genome-wide scan followed by positional cloning. A genome-wide scan of the Australian pedigree was carried out, followed by fine mapping and multipoint analysis in regions of interest (Chapter 5). The peak 2-point LOD scores from the genome-wide scan were LOD = 2.75 at D7S507 and LOD = 1.76 at D18S70. Two additional regions were also considered for fine mapping: chromosome 19p11-q13.1 with a LOD of 1.58 and chromosome 5q35-qter with a LOD of 1.57. Multipoint and haplotype analysis of markers flanking D7S507 did not support linkage to this region (Chapter 5). Similarly, fine mapping of chromosome 19p11-q13.1 failed to support linkage to this region (Chapter 5). Linkage analysis with additional markers in the region on chromosome 5q35-qter revealed a peak multipoint LOD score of 6.77 (Chapter 5). A distinct haplotype was shown to segregate with all members of the family, except the offspring of III-5 and III-6. Haplotype analysis of markers flanking D18S70 demonstrated a haplotype segregating with Paget's disease in a large sub-pedigree (descendants of III-3 and III-4) (Chapter 5). This sub-pedigree had a significantly lower age at diagnosis than the rest of the pedigree (51.2 + 8.5 vs. 64.2 + 9.7 years, p = 0.0012). Linkage analysis of this sub-pedigree demonstrated a peak two-point LOD score of 4.23 at marker D18S1390 (q = 0.00), and a peak multipoint LOD score of 4.71, at marker D18S70. An implication of these data is that 18q23 harbours a novel modifier gene for reducing the age of onset of Paget's disease of bone. A number of candidate Paget's genes have previously been identified on chromosome 18q23, including the nuclear factor of activated T cells (NFATc1), membrane-associated guanylated kinase (MAGUK) and a zinc finger protein. Candidate gene sequencing of these genes in these studies has failed to identify mutations segregating with affected family members in the sub-pedigree linked to chromosome 18q23 (Chapter 6). More recently, a mutation in the gene encoding the ubiquitin-binding protein sequestosome 1 (SQSTM/p62) has been shown to segregate with affected members of Paget's disease families of French-Canadian origin. In this study, a single base pair deletion (1215delC) was identified as segregating with the majority of affected members in the pedigree (Chapter 6). This deletion introduces a stop codon at amino acid position 392 which potentially results in early termination of the protein and loss of the ubiquitin binding domain. The three affected members of the family that do not share the affected haplotype do not carry a mutation in the coding region of SQSTM/p62. Screening of affected members from 10 further Paget's disease families identified the previously reported P392L mutation in 2 (20%) families. No SQSTM1/p62 coding mutations have been found in the remaining 8 families or in 113 aged matched controls. In conclusion, this project has identified genetic loci and mutations that segregate with individuals affected with Paget's disease. Further investigation of the functional significance of the genetic changes at these loci is expected to lead to a better understanding of the molecular basis of this disease.
15
Zhang, Yang. „Dynamic Memory Management for the Loci Framework“. MSSTATE, 2004. http://sun.library.msstate.edu/ETD-db/theses/available/etd-04062004-215627/.
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Resource management is a critical part in high-performance computing software. While management of processing resources to increase performance is the most critical, efficient management of memory resources plays an important role in solving large problems. This thesis research seeks to create an effective dynamic memory management scheme for a declarative data-parallel programming system. In such systems, some sort of automatic resource management is a requirement. Using the Loci framework, this thesis research focuses on exploring such opportunities. We believe there exists an automatic memory management scheme for such declarative data-parallel systems that provides good compromise between memory utilization and performance. In addition to basic memory management, this thesis research also seeks to develop methods that take advantages of the cache memory subsystem and explore balances between memory utilization and parallel communication costs in such declarative data-parallel frameworks.
16
Soni, Krunal Navinchandra. „Work replication a communication optimization for Loci /“. Master's thesis, Mississippi State : Mississippi State University, 2005. http://sun.library.msstate.edu/ETD-db/ETD-browse/browse.
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17
Carlborg, Örjan. „New methods for mapping quantitative trait loci /“. Uppsala : Dept. of Animal Breeding and Genetics, Swedish Univ. of Agricultural Sciences ([Institutionen för husdjurens genetik], Sveriges lantbruksuniv.), 2002. http://projkat.slu.se/SafariDokument/210.htm.
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18
Grenville, Laura Joy. „A virulence loci in Peronospora parasitica (At)“. Thesis, University of Birmingham, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399035.
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19
Coates, Mary Elizabeth. „Defining downy mildew (Hyaloperonospora parasitica) avirulence loci“. Thesis, University of Warwick, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441696.
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20
Martinez, de la Vega Octavio. „Quantitative trait loci estimation in plant populations“. Thesis, University of Reading, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.358346.
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21
McAdam, Rodney. „Tracing the loci of total quality management“. Thesis, University of Ulster, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393486.
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22
Logeswaran, Sayanthan. „Mapping quantitative trait loci in microbial populations“. Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/4881.
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Linkage between markers and genes that affect a phenotype of interest may be determined by examining differences in marker allele frequency in the extreme progeny of a cross between two inbred lines. This strategy is usually employed when pooling is used to reduce genotyping costs. When the cross progeny are asexual the extreme progeny may be selected by multiple generations of asexual reproduction and selection. In this thesis I will analyse this method of measuring phenotype in asexual cross progeny. The aim is to examine the behaviour of marker allele frequency due to selection over many generations, and also to identify statistically significant changes in frequency in the selected population. I will show that stochasticity in marker frequency in the selected population arises due the finite initial population size. For Mendelian traits, the initial population size should be at least in the low to mid hundreds to avoid spurious changes in marker frequency in the selected population. For quantitative traits the length of time selection is applied for, as well as the initial population size, will affect the stochasticity in marker frequency. The longer selection is applied for, the more chance of spurious changes in marker frequency. Also for quantitative traits, I will show that the presence of epistasis can hinder changes in marker frequency at selected loci, and consequently make identification of selected loci more difficult. I also show that it is possible to detect epistasis from the marker frequency by identifying reversals in the direction of marker frequency change. Finally, I develop a maximum likelihood based statistical model that aims to identify significant changes in marker frequency in the selected population. I will show that the power of this statistical model is high for detecting large changes in marker frequency, but very low for detecting small changes in frequency.
23
Prevette, David Anderson. „Seven Loci: The Completion of Villa Maderni“. Thesis, Virginia Tech, 2003. http://hdl.handle.net/10919/10046.
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Through observation and critical response, Seven Loci: The Completion of Villa Maderni is for the author not only a work reflective of his still emergent design judgments, but also one birthed as he lived and worked in the physical fabric of the place. The primary goal of this work is to propose an inhabitable enclosure for the perimeter of an already sacred villa and garden in the Ticino region of Switzerland. The secondary goal of the thesis is to explore and propose an architecture which does not make a forgery of the villa, but one whose language is of its own time and materials, all the while responding to the invisible traditions of the town, street and site.Master of Architecture
24
Whang, Jamie Jung-A. „An Urban Monastery and Its Genius Loci“. Thesis, Virginia Tech, 2002. http://hdl.handle.net/10919/43410.
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Genius loci has been described as "the spirit of place". The main interest in considering an urban monastery program is to create a place that embodies the spirit and culture of Tibetan Buddhism in the context of urban Washington, D.C. Given Tibet's unique culture that has developed over centuries without much Western influence, and it recent history of Chinese rule, religious persecution and infiltration of its language, culture and environment, the challenge of this program is to represent the traditions of Tibetan Buddhism in a modern language of architecture.Master of Architecture
25
Yang, Jie. „Nonparametric functional mapping of quantitative trait loci“. [Gainesville, Fla.] : University of Florida, 2006. http://purl.fcla.edu/fcla/etd/UFE0014762.
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Roberts, Simon Benedict. „Investigating new genetic susceptibility loci in osteoarthritis“. Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/28982.
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Primary osteoarthritis (OA) is a late-onset, degenerative condition of synovial joints, and is the major cause of pain and disability in older persons. OA represents a significant disease burden and focus of research, especially as no disease-modifying therapies exist to manage the condition. The genetic influence to OA is complex and polygenic. The arcOGEN study, the most powerful genome-wide association study yet to investigate OA in humans, identified the 9q33.1 locus to be significantly associated with hip OA in females. TRIM32 lies within the 9q33.1 susceptibility locus and may have strong biological relevance to OA; it encodes a protein with E3 ubiquitin ligase activity. Sanger sequencing of TRIM32 in the youngest 500 female patients with hip OA from the arcOGEN study was performed to identify rare variants in TRIM32 that are associated with OA of the hip in females. Polymorphisms were identified in the proximal promoter, and 3’untranslated regions (3’UTR) of TRIM32 that are disproportionately represented in female patients with hip OA, compared to the control population. In vitro studies identified expression of TRIM32 in human femoral head cartilage; reduced expression of TRIM32 was also demonstrated in femoral head primary articular chondrocytes from patients with hip OA compared to control patients. Trim32 knockout resulted in increased aggrecanolysis in murine femoral head explants. Murine chondrocytes deficient in Trim32 also exhibited increased expression of markers of a mature chondrocyte phenotype in response to anabolic cytokine stimulation, and increased expression of markers of a hypertrophic chondrocyte phenotype upon catabolic cytokine stimulation. In vivo studies of joint degeneration in Trim32 knockout mice demonstrated increased cartilage degradation and tibial epiphyseal bone changes after surgically induced knee joint instability, compared to wild-type mice. Increased cartilage degradation and medial knee subchondral bone changes were also identified upon ageing of Trim32 knockout mice. These results further implicate TRIM32 in the genetic predisposition to OA, and indicate a role for TRIM32 in the joint degeneration evident in OA. These results support the further study of TRIM32 in the pathophysiology of OA and development of novel therapeutic strategies to manage OA.
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Good, David Andrew. „Genetic Loci for Paget's Disease of Bone“. Thesis, Griffith University, 2003. http://hdl.handle.net/10072/365759.
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Paget's disease of the bone is a skeletal disorder of unknown cause. This disease is characterised by excessive and abnormal bone remodelling brought about by increased bone resorption followed by disorganised bone formation. Increased bone turnover results in a disorganised mosaic of woven and lamellar bone at affected skeletal sites. This produces bone that is expanded in size, less compact, more vascular, and more susceptible to deformity or fracture than normal bone. Symptoms of Paget's disease may include bone pain, bone deformity, excessive warmth over bone from hypervascularity, secondary arthritis, and a variety of neurologic complications caused in most instances by compression of the neural tissues adjacent to pagetic bone. Genetic factors play a role in the pathogenesis of Paget's disease but the molecular basis remains largely unknown. The identification of the molecular basis of Paget's disease is fundamental for an understanding of the cause of the disease, for identifying subjects at risk at a preclinical stage, and for the development of more effective preventive and therapeutic strategies for the management of the condition. With this in mind, the aim of this project is to identify genetic loci, in a large pedigree, that may harbour genes responsible for Paget's disease of bone. A large Australian family with evidence of Paget's disease was recruited for these studies (Chapter 3). This pedigree has characterised over 250 individuals, with 49 informative individuals affected with Paget's disease of bone, 31 of whom are available for genotypic analysis. The pattern of disease in these individuals is polystotic, with sites of involvement including the spine, pelvis, skull and femur. Although the affected individuals have a severe early-onset form of the disease, the clinical features of the pedigree suggest that the affected family members have Paget's disease and not familial expansile osteolysis (a disease with some similarities to Paget's disease), as our patients have extensive skull and axial skeletal involvement. The disease is inherited as an autosomal dominant trait in the pedigree with high penetrance by the sixth decade. Due to the large size of this family and multiple affected members, this pedigree is a unique resource for the detection of the susceptibility gene in Paget's disease. The first susceptibility loci for Paget's disease of bone have been mapped by other investigators to chromosome 6p21 (PDB1) and 18q21.1-q22 (PDB2) in different pedigrees. Linkage analysis of the Australian pedigree in these studies was performed with markers at PDB1: these data showed significant exclusion of linkage, with LOD scores < - 2 in this region (Chapter 4). Linkage analysis of microsatellite markers from the PDB2 region excluded linkage with this region also, with a 30 cM exclusion region (LOD score < -2.0) centred on D18S42 (Chapter 4). This locus on chromosome 18q21.1-q22 contains a serine protease (serpin) cluster with similarities to chromosome 6p21. Linkage analysis of this region also failed to provide evidence of linkage to this locus (Chapter 4). These data are consistent with genetic heterogeneity of Paget's disease of bone. A gene essential for osteoclast formation encoding receptor activator of nuclear factor-kB (RANK), TNFRSF11A, has been previously mapped to the PDB2 region. Mutations in the TNFRSF11A gene have been identified segregating in pedigrees with Familial Expansile Osteolysis and early onset familial Paget's disease, however, linkage studies and mutation screening have excluded the involvement of RANK in the majority of Paget's disease patients. For the Australian pedigree, mutation screening at the TNFRSF11A locus revealed no mutations segregating with affected individuals with Paget's disease (Chapter 4). Based on these findings, our hypothesis is that a novel susceptibility gene relevant to the pathogenesis of Paget's disease of bone lies elsewhere in the genome in the affected members of this pedigree; this gene should be identifiable using a microsatellite genome-wide scan followed by positional cloning. A genome-wide scan of the Australian pedigree was carried out, followed by fine mapping and multipoint analysis in regions of interest (Chapter 5). The peak 2-point LOD scores from the genome-wide scan were LOD = 2.75 at D7S507 and LOD = 1.76 at D18S70. Two additional regions were also considered for fine mapping: chromosome 19p11-q13.1 with a LOD of 1.58 and chromosome 5q35-qter with a LOD of 1.57. Multipoint and haplotype analysis of markers flanking D7S507 did not support linkage to this region (Chapter 5). Similarly, fine mapping of chromosome 19p11-q13.1 failed to support linkage to this region (Chapter 5). Linkage analysis with additional markers in the region on chromosome 5q35-qter revealed a peak multipoint LOD score of 6.77 (Chapter 5). A distinct haplotype was shown to segregate with all members of the family, except the offspring of III-5 and III-6. Haplotype analysis of markers flanking D18S70 demonstrated a haplotype segregating with Paget's disease in a large sub-pedigree (descendants of III-3 and III-4) (Chapter 5). This sub-pedigree had a significantly lower age at diagnosis than the rest of the pedigree (51.2 + 8.5 vs. 64.2 + 9.7 years, p = 0.0012). Linkage analysis of this sub-pedigree demonstrated a peak two-point LOD score of 4.23 at marker D18S1390 (q = 0.00), and a peak multipoint LOD score of 4.71, at marker D18S70. An implication of these data is that 18q23 harbours a novel modifier gene for reducing the age of onset of Paget's disease of bone. A number of candidate Paget's genes have previously been identified on chromosome 18q23, including the nuclear factor of activated T cells (NFATc1), membrane-associated guanylated kinase (MAGUK) and a zinc finger protein. Candidate gene sequencing of these genes in these studies has failed to identify mutations segregating with affected family members in the sub-pedigree linked to chromosome 18q23 (Chapter 6). More recently, a mutation in the gene encoding the ubiquitin-binding protein sequestosome 1 (SQSTM/p62) has been shown to segregate with affected members of Paget's disease families of French-Canadian origin. In this study, a single base pair deletion (1215delC) was identified as segregating with the majority of affected members in the pedigree (Chapter 6). This deletion introduces a stop codon at amino acid position 392 which potentially results in early termination of the protein and loss of the ubiquitin binding domain. The three affected members of the family that do not share the affected haplotype do not carry a mutation in the coding region of SQSTM/p62. Screening of affected members from 10 further Paget's disease families identified the previously reported P392L mutation in 2 (20%) families. No SQSTM1/p62 coding mutations have been found in the remaining 8 families or in 113 aged matched controls. In conclusion, this project has identified genetic loci and mutations that segregate with individuals affected with Paget's disease. Further investigation of the functional significance of the genetic changes at these loci is expected to lead to a better understanding of the molecular basis of this disease.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
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Chilakamarri, Sunita R. „Genetic differentiation in Alewife populations using microsatellite loci“. Link to electronic thesis, 2005. http://www.wpi.edu/Pubs/ETD/Available/etd-053105-164623/.
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Xu, Chun. „Candidate genes and chromosomal loci in multiple sclerosis /“. Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3433-9/.
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Cox, William E. „Towards a genius loci : Atlanta architecture and urbanism“. Thesis, Georgia Institute of Technology, 1992. http://hdl.handle.net/1853/30739.
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Papaemmanuil, Elli. „The identification of novel colorectal cancer susceptibility loci“. Thesis, Institute of Cancer Research (University Of London), 2009. http://publications.icr.ac.uk/10464/.
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Colorectal cancer (CRC) is the second most common malignancy in developed countries. Germline mutations in a number of genes have been shown to cause CRC, but the Mendelian syndromes associated with these known genes (APC, DNA mismatch repair genes, MYH, SMAD4, ALK3 and STK11) account for less than 5% of the familial clustering. Colorectal tumor families which show evidence against linkage to known disease loci, provide direct evidence for the existence of uncharacterized high/moderate-penetrance CRC genes. Such observations strongly support the continued search for novel CRC predisposition genes through genome-wide linkage. To identify novel CRC susceptibility genes through linkage analyses a series of CRC families in which involvement of known susceptibility genes has been excluded were ascertained. Genome-wide genotyping was performed using high-density SNP arrays to provide maximal power to detect linkage. This study provided statistically significant evidence for a novel predisposition locus for CRC mapping to 3q21-24. Using a series of microsatellite markers the critical interval of linkage was refined to 1 4.4Mb region at 3q22. To further investigate Mendelian susceptibility to CRC, a search for a disease gene at 3q22 was performed by linkage disequilibrium (LD) mapping in 620 familial CRC cases and 960 controls, genotyping 1,676 tagging SNPs and sequencing 30 candidate genes from the region. Signal intensity data from the SNP markers was further evaluated for structural variation within 3q22. On the bases of LD mapping, chromosomal profiling and mutational analyses of genes mapping to 3q22, no causal mutation was identified. Findings are consistent with the hypothesis that variation at 3q22 contributes to a significant proportion of the unexplained genetic risk to CRC, however this is unlikely to be mediated through a restricted set of alleles and is refractory to identification by current analyses strategies.
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McEwen, Kirsten Rose. „Epigenetic regulation of imprinted loci in the mouse“. Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609297.
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Seemungal, Barry Mitra. „The mechanisms and loci of human vestibular perception“. Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1445054/.
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This thesis' primary aims were to characterise the what, where and how of vestibular cortical processing. A secondary aim was to assess the effects of early visual deprivation on vestibular perception, in particular the what and where.;The What: Using an angular vestibular navigation paradigm with physiological range stimuli, we quantitatively demonstrated that healthy subjects were able to actively reproduce spatial and kinetic parameters of a passively travelled trajectory (displacement, time, velocity and acceleration). Early blind subjects showed no deficit in the perception of raw vestibular signals but were relatively impaired in more complex spatial vestibular navigation tasks. Congenitally blind subjects did not show the normal prolongation of the vestibular signal coming from the labyrinth (i.e. velocity storage mechanism) at perceptual level and two blind subjects who had superior navigational ability also had ultra-short vestibular time constants. Based upon a questionnaire assessment of these subjects, we concluded that frequent exposure to specific activities (e.g. down-hill skiing for one subject!) may be protective in allowing a normal navigational capacity in these subjects. The mechanism for the ultra-short time constants and their role in superior navigational performance remains unclear.;The Where: Using repetitive transcranial stimulation (rTMS) to the right posterior parietal cortex we disrupted the perceptual encoding of vestibular signals during a passive yaw-plane rotation. We found no effect of rTMS on vestibular encoding with occipital cortical stimulation in sighted or blind subjects.;The How: We hypothesised that vestibular signals may be encoded via an internal model at perceptual level. Using a novel paradigm, we found that by perturbing the internal estimate of displacement of a previously travelled trajectory (yaw plane rotation), we could alter the perception of motion duration but not velocity, of the rotation, a finding consistent with our hypothesis. The last experiment in this thesis was developed in an attempt to bridge the gap between brainstem and perceptual vestibular function. We quantitatively show that brainstem thresholds to angular acceleration are lower than for cortical (perceptual) thresholds. The hypothesis that we aim to test in the future is that patients who show a large dichotomy between brainstem and cortical thresholds to angular acceleration may be either objectively compromised by worse balance function or subjectively worse as defined by their symptoms of dizziness and disorientation.
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Ahmed, Helal Uddin. „Mapping stress tolerance genetic loci in Arabidopsis thaliana“. Thesis, University of Newcastle Upon Tyne, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246628.
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Parsons, Claire A. „Investigation of loci influencing osteoporosis using DNA pooling“. Thesis, University of Aberdeen, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408968.
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A major predictor of osteoporotic fracture is bone mineral density (BMD), and BMD variance has been shown through twin and family studies to be determined genetically in some cases up to 85% (the majority of genes as yet undefined). Attempts to identify these genes has proved challenging, genome-wide linkage studies have located a large number of BMD influencing loci (quantitative trait loci (QTLs)) but these regions usually remain large 1030 cM, subsequently requiring fine mapping to find positional candidate genes. The need for large scale genotyping studies is necessary to find genes which exert modest effects like those thought to act upon BMD regulation, in this thesis I show how DNA pooling of cases (low BMD) and controls (high BMD) can be compared to look for significant differences in allelic distribution. As different loci have been linked with different skeletal sites, two DNA pool sets were constructed one for lumbar spine (LS) BMD and the other for femoral neck (FN) BMD. The DNA pools were utilised to assess if five single nucleotide polymorphisms (SNPs) in a monogenic bone disease gene (SOST) influence normal LS BMD regulation, in this study the SOST SNP’s were shown to have no influence on LS BMD regulation, however the DNA pools were shown to successfully predict allele frequencies of the individuals pooled using PyrosequencingTM but not using direct sequencing methods. A LS BMD QTL localised in a mouse and then the syntenic human region (Xp22) was located and fine mapped using DNA pools, this successfully showed that the human QTL influenced LS BMD and narrowed the potential candidate genes to just six. Thus validating the use of cross-species research in the elucidation of complex diseases using DNA pooling and linkage disequilibrium mapping.
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Zaffaroni, Daniela. „Mapping of skin cancer susceptibility loci in mice“. Thesis, Open University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270016.
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Martin, Jolyon Nicolas Edouard. „Functional analyses of the canine antigen receptor loci“. Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/282874.
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Udler, Miriam. „Fine-scale mapping of breast cancer susceptibility loci“. Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611732.
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Armour, John Anthony. „The isolation and characterization of human minisatellite loci“. Thesis, University of Leicester, 1990. http://hdl.handle.net/2381/35423.
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Hypervariable minisatellite regions of human DNA are of considerable interest, not only as highly informative genetic systems, but also as intermediately sized regions of tandem repetition. Methods for the isolation of minisatellite loci from the human genome have been investigated, and 23 new hypervariable loci cloned from an ordered array Charomid library. This method not only allows very efficient isolation of human minisatellites, but can also be used to observe the degree of overlap between multi-locus DNA fingerprinting probes. The 23 new loci have a mean heterozygosity level of 71%, and have been characterized and mapped in the genome. The genomic disposition of human minisatellites has been analysed by investigation of cloned examples. The minisatellites studied show a strong tendency to cluster near the ends of chromosomes, and sequence analysis demonstrates a significant excess of dispersed repeat elements in the DNA flanking human minisatellites. Minisatellite variant repeat (MVR) mapping has also been used to investigate the internal structure of minisatellite alleles. Somatic allele length mutation events have been demonstrated in DNA from colorectal adenocarcinomas, and the mutations observed show many features of general similarity to germline mutation events. A series of human breast tumours has been screened for somatic change, using both multi-locus DNA fingerprinting probes and single-locus minisatellite probes. Somatic change in breast cancers is much less frequent than in colorectal tumours, but some allele losses and mutations have been defined, including a highly unusual mutation, which may be the result of a minisatellite transposition event. Finally, evolution at minisatellite loci has been studied, both by examination of allelic states in current human populations, as well as comparison with non-human primates.
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Greenshields, David. „Isolation of adaptive quantitative trait loci in Antirrhinum“. Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/14950.
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Understanding the genetic basis of quantitative traits represents a huge goal in modern molecular and evolutionary biology. Here, the natural genetics of the genus Antirrhinum, within which separate species can be successfully interbred, are used to investigate differences in a range of morphological characteristics. The two species used in the study, Antirrhinum majus and Antirrhinum molle, have become adapted to very diverse environments and consequently exhibit large variance in a wide range of traits. A large-scale FI mutant screen, from a cross between a transposon-active A. majus line and A. molle, isolated segregating mutations for flower size, flower colour, trichome density and branching in self-pollinated F2 populations. Amplified Fragment Length Polymorphism analysis of the F2 and the use of molecular maps have shown the mutations generally correspond to known Quantitative Trait Loci, and the roles of genes linked to these regions are discussed. The technique sheds some light on the molecular and evolutionary mechanisms underpinning diversity in Antirrhinum and has implications for the use of transposon-tagging in locating QTL in other plant systems.
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Ritchey, Brian Michael. „Quantitative Trait Loci Mapping Of Macrophage Atherogenic Phenotypes“. Cleveland State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=csu1510080975338565.
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Dorajoo, Rajkumar. „Detection of novel obesity loci in Asian populations“. Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/10142.
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Genome-wide association studies (GWAS) have successfully identified common obesity-associated variants. These have been primarily conducted using populations of European ancestry and the relevance of these loci in other populations remains to be determined. The aims of this study were multi-fold, in both corroborating the role of these variants in Asians and in unravelling new obesity-associated variants. In my first study, I examined the relevance of specific variants, initially identified in Europeans, with obesity in Asian populations from Singapore (Chinese, Malays and South-Asians). This confirmed the role of several novel obesity loci and suggested that common variants obesity-associated variants were relevant across ethnic groups. To identify additional obesity-associated loci in East-Asians, a hypothesis-free GWAS approach was adopted in the next study. These studies were initially carried out in Singaporean datasets and subsequently, expanded to consortia levels to increase power in the study. These efforts successfully identified novel BMI-associated variants in East-Asians and highlighted that insulin-associated processes may be involved in obesity susceptibility. In the third study I extended the findings of a possible role for insulin-associated processes in obesity by aiming to understand the relevance of type 2 diabetes risk loci with obesity predisposition in adults and in childhood and birth among East-Asian datasets. Data from this study revealed a possible ethnic-specific association at a HHEX locus among adult East-Asians and identified another HHEX variant at which the effects on childhood BMI interacted with birth weight. In the final study, I assessed an inflammatory phenotype, serum C-reactive protein levels, for novel associations in East-Asian datasets using GWAS with a focus on identifying any obesity interactions. I further sought to clarify on the causality between CRP with vascular disease in this study. Although no novel variants were detected in this study, several initial findings from earlier GWAS were replicated in the East-Asian populations. Furthermore, it was determined that CRP was not causally associated with macrovascular and microvascular disease. Primary results from these studies served to replicate several novel obesity loci in Asian populations and revealed novel risk variants. Nevertheless, it is striking that much of the genetic variation in obesity levels remains unidentified. Additional research is necessary to pin-point causal location and mechanisms for the already identified loci and it would be important to address the role of non-SNP genetic variations in obesity susceptibility.
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Sethuraman, Swaminathan. „Volumes of certain loci of polynomials and their applicatoins“. [College Station, Tex. : Texas A&M University, 2009. http://hdl.handle.net/1969.1/ETD-TAMU-2009-05-787.
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Schwarz, Sebastean. „Kartierung von Loci für kongenitales Ausgrätschen beim neugeborenen Ferkel /“. Kiel : Selbstverlag des Instituts für Tierzucht und Tierhaltung der Christian-Albrechts-Universität zu Kiel, 2003. http://e-diss.uni-kiel.de/diss_827/d827.pdf.
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Bao, Haikun. „Bayesian hierarchical regression model to detect quantitative trait loci /“. Electronic version (PDF), 2006. http://dl.uncw.edu/etd/2006/baoh/haikunbao.pdf.
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Cosentino, Lidia. „A comparison of transgenic and endogenous loci in vivo“. Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0018/NQ56223.pdf.
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Gong, Xiaohua. „Mapping Quantitative Trait Loci in Outbred Half-sib Populations“. NCSU, 2009. http://www.lib.ncsu.edu/theses/available/etd-05042009-160015/.
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Quantitative trait loci (QTL) mapping in outbred populations faces some challenges unique to the divergent genetic background and complex pedigree relationships. Motivated by a dairy cattle half-sib data set from a grand daughter design, we present in this dissertation a series of endeavors to address various challenges along the analysis flow of QTL mapping. A first step is to infer the haplotypes in sires based on the observed genotypes in sires and his offspring. Our method was shown to outperform peer methods with greater robustness and accuracy yet with fast speed performance. Then in light of adapting the multiple interval mapping method to within-family QTL analysis, we extended the modeling framework by allowing for heteroscedastic residual variances and upgraded the Windows QTL Cartographer accordingly. The advantageous post-analysis result parsing from Windows QTL Cartographer and more importantly, the improved analysis outputs due to more powerful maximum likelihood-based mixture modeling than the least squares regression manifest our efforts in delivering better methodology via practically user friendly software. We further developed a mixed model approach for the purpose of QTL mapping across multiple families that was aimed at modeling QTL effects as both the fixed effect across families and the random effect within families. Our mixed model was shown to encompass similar or higher statistical testing performance on QTL variation than the widely used variance component modeling approach, yet still allowing permutations for obtaining chromosome-wide or genome-wide significance threshold. What's more, the flexibility of our mixed model in constructing alternative hypotheses testing on either fixed or random QTL effects or both was shown to offer interesting insight into the varying sources of signal that would not be unveiled by least squares regression or variance component methods. In concluding our comprehensive approach to QTL linkage mapping in dairy cattle populations, we continue to explore methods of fine mapping by combining both the linkage disequilibrium and linkage information and prospective method improvements are being sought.
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Schwarz, Sebastean. „Kartierung von Loci für kongenitales Ausgrätschen beim neugeborenen Ferkel“. Kiel Inst. für Tierzucht und Tierhaltung, 2002. http://e-diss.uni-kiel.de/diss_827/d827.pdf.
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Marklund, Lena. „Genome analysis of quantitative trait loci in the pig /“. Uppsala : Swedish Univ. of Agricultural Sciences (Sveriges lantbruksuniv.), 1997. http://epsilon.slu.se/avh/1997/91-576-5416-6.gif.
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Törnsten, Anna. „Physical mapping of important trait loci in the pig /“. Uppsala : Swedish Univ. of Agricultural Sciences (Sveriges lantbruksuniv.), 2000. http://epsilon.slu.se/avh/2000/91-576-5913-3.pdf.
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