Cette these presente une etude du modele XY bidimensionnel dans des conditions realistes, comme la presence d'imperfections (impuretes non magnetiques) ou la taille finie du reseau. Ces deux aspects sont typiques de situations experimentales et necessitent un questionnement theorique. Nous avons egalement considere le comportement a basse temperature du modele d'Heisenberg fini et avons trouve un comportement analogue a celui du modele XY. Nous avons utilise a la fois une approche analytique et des simulations numeriques pour traiter le probleme. Les resultats essentiels de ce travail sont : (a) la determination de l'exposant de decroissance algebrique de la fonction de correlation du modele XY dilue, analytiquement avec l'approximation d'ondes de spins et par simulations Monte Carlo a l'aide de l'algorithme de Wolff, (b) l'estimation correspondante dans le cas du modele d'Heisenberg sur reseau fini a basse temperature assortie de simulations numeriques egalement, (c) la forme de l'interaction entre les impuretes non magnetiques et les defauts topologiques dans le cadre du modele de Villain et dans le modele de Kosterlitz-Thouless, et l'estimation analytique de la reduction de temperature critique basee sur la forme de cette interaction, (d) la determination numerique de la distribution de probabilite de l'aimantation residuelle sur un systeme fini en presence de desordre. Pour l'ensemble de nos travaux, nous avons obtenu un bon accord entre les predictions theoriques et les simulations numeriques, de meme qu'avec des travaux anterieurs le cas echeant.

No description available.

No description available.

In this thesis we study the connection between continuum quantum field theory and corresponding lattice field theory, specifically for two cases: Landau gauge fixing and ’t Hooft-Polyakov monopoles. To study non-perturbative phenomena such as the confinement mechanism of quarks and gluons and dynamical chiral symmetry breaking in Quantum Chromodynamics (QCD), there are two major approaches: the Dyson-Schwinger equations (DSEs) approach, which is based on the covariant continuum formulation, and lattice gauge theory. The strength and beauty of lattice gauge theory is due to the fact that gauge invariance is manifest and fixing a gauge is not required. In the covariant continuum formulation of gauge theories, on the other hand, one has to deal with the redundant degrees of freedom due to gauge invariance and has to fix gauge (most popularly, Landau gauge). There, the gauge-fixing machinery is based on the so-called Faddeev-Popov procedure or more generally, the Becchi-Rouet-Stora-Tyutin (BRST) symmetry. Beyond perturbation theory this is aggravated by the existence of so-called Gribov copies, however, that satisfy the same gauge-fixing condition, but are related by gauge transformations, and are thus physically equivalent. When attempting to fix Landau gauge on the lattice to make a connection with its continuum counterpart, this ambiguity manifests itself in the Neuberger 0/0 problem that asserts that the expectation value of any physical observable will always be of the indefinite form 0/0. We explain the topological nature of this problem and how the complete cancellation of Gribov copies can be avoided in a modified lattice Landau gauge based on a new definition of gauge fields on the lattice as stereographically projected link variables. For compact U(1), where the Gribov copy problem is related to the classification the local minima of XY spin glass models, we explicitly show that there still remain Gribov copies but their number is exponentially reduced in lower dimensional models. We then formulate the corresponding Faddeev-Popov procedure on the lattice, for these models. Moreover, we explicitly demonstrate that the proposed modification circumvents the Neuberger 0/0 problem for lattices of arbitrary dimensions for compact U(1). Applied to the maximal Abelian subgroup this will avoid the perfect cancellation amongst the remaining Gribov copies for SU(N), and so the corresponding BRST formulation is also then possible for generic SU(N), in particular, for the Standard Model groups. For higher dimensional lattices, the gauge fixing conditions for both the standard and the modified lattice Landau gauges are systems of multivariate nonlinear equations, solving which in general is a highly non-trivial task. However, we show that these systems can be interpreted as systems of polynomial equations. They can then be solved exactly by computational Algebraic Geometry, the Groebner basis technique in particular, and numerically by the Polynomial Homotopy Continuation method. ’t Hooft-Polyakov monopoles play an important role in high energy physics due to their presence in grand unified theories and their usefulness in studying non-perturbative properties of quantum field theories through electric-magnetic dualities. In the second part of the thesis, we study adjoint Higgs models, which exhibit ’t Hooft-Polyakov monopoles, and have been extensively analyzed using semi-classical analysis in the continuum. However, to study them in a fully nonperturbative fashion, it is essential to put the theory on the lattice. Here, we investigate twisted C-periodic boundary conditions in SU(N) gauge field theory with an adjoint Higgs field and show that for even N with a suitable twist one can impose a non-zero magnetic charge relative to each of N − 1 residual U(1)’s in the broken phase, thereby creating ’t Hooft-Polyakov magnetic monopoles. This makes it possible then to use lattice Monte-Carlo simulations to study the properties of these monopoles in the full quantum theory and compare them with the existing results in the continuum. / Thesis (Ph.D.) -- University of Adelaide, School of Chemistry and Physics, 2010

Submitted by Barroso Patrícia (barroso.p2010@gmail.com) on 2014-08-16T18:09:29Z No. of bitstreams: 1 MOTA, Bianca Costa.pdf: 1950610 bytes, checksum: cf1c3d3f181fbc2ecd92f0663fd6675c (MD5) / Made available in DSpace on 2014-08-16T18:09:29Z (GMT). No. of bitstreams: 1 MOTA, Bianca Costa.pdf: 1950610 bytes, checksum: cf1c3d3f181fbc2ecd92f0663fd6675c (MD5) / Introdução: O termo DDS refere-se aos distúrbios que afetam o processo normal de desenvolvimento e diferenciação sexual,os quais podem ou não se manifestar sob a forma de genitália ambígua,levando a discordância entre o sexo cromossômico, gonadal e fenotípico.A incidência estimada desses distúrbios é de umpara 4500-5500 nascimentos. Os indivíduos com DDS e cariótipo 46,XY apresentam virilização deficiente da genitália externa, que pode decorrer dehipoplasia das células de Leydig, alterações enzimáticas na síntese de testosterona, deficiência da enzima 5α-redutase, disgenesiasgonadais, anorquia, síndrome da insensibilidade androgênica ou DDS ovotesticular. Objetivo: Este trabalho teve como objetivo descrever o perfil clínico e epidemiológico de pacientes DDS 46,XY matriculados e acompanhados no Ambulatório de DDS do Hospital Universitário Professor Edgard Santos da Universidade Federal da Bahia. Metodologia: Trata-se de um estudo retrospectivo com revisão de prontuários dos pacientes com DDS 46,XY incluídos no banco de dados do referido ambulatório. Após análise desse banco de dados, foram selecionados todos os 122 pacientes com diagnóstico sindrômico de DDS 46,XY. Resultados: Foram estudados 110 pacientes; 47 deles não tinham diagnóstico etiológico; 16,apresentavam deficiência de 5α- redutase; 19, síndrome da insensibilidade androgênica. Na primeira consulta, a mediana da idade foi de 1,6 anos, 76 indivíduos eram do sexo masculino, 31 do sexo feminino e 03 ainda não tinham registro civil. Dois pacientes com registro civil feminino mudaram de gênero para o masculino durante o acompanhamento. Setenta e quatro pacientes foram encaminhados por apresentarem genitália ambígua ou criptorquidia. No grupo estudado, 73,6% tinham gônadas palpáveis.Entre os 47 pacientes sem diagnóstico etiológico, 87% foram registrados no sexo masculino. A gonadectomia e a uretoplastia foram as cirurgias mais realizadas, e 47% dos pacientes não realizaram qualquer tipo de cirurgia. Conclusão: As etiologias mais comuns foram: síndrome da insensibilidade androgênica (17%), deficiência de 5α-redutase (15%) e disgenesiasgonadais (6%). O diagnóstico etiológico não foi possível em 43% dos pacientes. A primeira avaliação ocorreu antes dos dez anos de idade em mais de 50% dos casos. Todos os pacientes com diagnóstico de síndrome da insensibilidade androgênica completa e 11 com deficiência de 5α-redutase foram registrados no gênero feminino. O motivo principal de encaminhamento foi a presença de ambiguidade genital. Todos os pacientes estudados estavam cadastrados no serviço de referência, e62% deles continuavam sendo acompanhados. O perfil clínico dos pacientes estudados está de acordo com os achados na literatura.

Made available in DSpace on 2014-12-17T15:15:01Z (GMT). No. of bitstreams: 1 SelmaRV_DISSERT.pdf: 2852447 bytes, checksum: 2b9488e49475092749d00972ff6c30bf (MD5) Previous issue date: 1994-05-27 / Coordena??o de Aperfei?oamento de Pessoal de N?vel Superior / Consideramos um vidro de spins misto definido em termos de dois grupos constitu?dos respectivamente, por vari?veis de tipo XY e planares discretas ( rel?gio com p-estados); apenas intera??es entre grupos distintos, do tipo alcance infinito, s?o permitidas. Um par?metro de anisotropia Dp que privilegia p dire??es no plano ? introduzido para as vari?veis XY, de tal forma a nos permitir uma interpola??o entre os modelos XY (Dp = 0 ; p = ∞ ) e rel?gio p-estados (Dp = ∞). Analisamos o procedimento de quebra da simetria entre r?plicas, onde diferentes tipos de fun??es par?metro de ordem s?o estudadas

The vortex fluctuations have proved to be responsible for the onset of dissipation in thin type-II superconducting Aims. There is also growing evidence that dissipation in high- temperature superconductors exhibits the same kind of two-dimensional (2D) behavior. However, a proper analysis of these materials requires a thorough understanding of the two-dimensional fluctuations. This thesis may be considered to consist of two parts. The first is concerned with two models that have often been used as models for 2D superconductors, the 2D Coulomb gas and the 2D XY model. The second part contains analyses related to high-temperature sup er conductivity. Through analysis of some renormalization equations for the Kosterlitz-Thouless (KT) transition, it is shown that the region governed by the KT critical behavior is very small and only applies at very low values for the flux-flow resistance. It is concluded that this critical behavior not is observable in superconductors, and, furthermore, that the only available method to test for 2D fluctuations at the onset of resistance, is through comparison with the 2D resistance scaling function. The critical temperature for the 2D XY model is determined by means of a finite- size scaling relation for the helicity modulus. The linearly screened potential in the XY model is written in terms of a correlation function. The analogy to the 2D Coulomb gas is found to be exact with a temperature-dependent bare interaction and a new expression for vorticity. It is also demonstrated that the Coulomb gas scaling concept may be applied to XY-type models. An analysis of resistance data for YBCO/PBCO superlattices in terms of the 2D resistance scaling function gives evidence for 2D behavior in the cases with large separation of the superconducting layers. In the superlattices with stronger interlayer coupling, the crossover to three-dimensional behavior is seen as a deviation from the scaling function as Tc is approached from above. The anisotropic three-dimensional (3D) XY model is examined as a model for high- temperature superconductors. It is shown that the density of vortices above Tc are closely equal in the anisotropic 3D model and the 2D model. This is taken as evidence that the 3D to 2D crossover found in the superlattices also is present in the anisotropic 3D XY model. / digitalisering@umu.se

Introdução: Várias evidências em estudos de animais knockout sugerem a efetiva participação dos genes Fgf9-Fgfr2 no processo de determinação testicular. Animais XY knockout para os genes Fgf9 e Fgfr2 apresentam reversão sexual como consequência da alteração na cascata de eventos masculinizantes nas gônadas fetais. Até o momento, mutações inativadoras dos genes FGF9-FGFR2 não foram descritas em pacientes 46, XY portadores de disgenesia gonadal. Objetivos: Pesquisar a presença de mutações inativadoras nos genes FGF9 e FGFR2 em pacientes portadores de DDS 46,XY por anormalidades do desenvolvimento gonadal. Casuística e Métodos: Trinta e três pacientes com disgenesia gonadal 46, XY, 11 com a forma completa e 22 com a forma parcial. As regiões codificadoras dos genes FGF9 e FGFR2 de todos os pacientes foram amplificadas e sequenciadas. As investigações quanto a presença de deleções foram realizadas usando-se a técnica de MLPA (Multiplex ligation-dependent probe amplification). Resultados: Mutações ou deleções nos genes FGF9 não foram encontradas em nenhum dos pacientes estudados, apenas alguns polimorfismos previamente descritos. No gene FGFR2 não foram encontradas deleções. Uma nova variante não sinônima em heterozigose, c.1358 C>T (p.Ser453Leu), localizada no exon 10 do FGFR2 foi encontrada em duas irmãs com disgenesia gonadal parcial 46,XY. A mãe é portadora da variante alélica e o estudo de 147 indivíduos controles não identificou a presença desta variante. A análise da variante em sites de previsão, PolyPhen, SIFT e Mutation Taster indicou que a nova proteína FGFR2 é possivelmente danificada. Conclusões: Se esses resultados dos sites de previsão forem confirmados em estudos funcionais futuros a participação do gene FGFR2 na determinação gonadal masculina em humanos estará comprovada / Introduction: Several evidence in animal studies \"knockout\" suggest the effective participation of Fgf9-Fgfr2 genes in testicular determination process. Animals XY \"knockout\" for Fgf9 and Fgfr2 genes exhibit sex reversal as a result of the change in the cascade of masculinizing events in fetal gonads. To date, So far inactivating mutations of FGF9 and FGFR2 genes have not been described in 46,XY patients with gonadal dysgenesis. Objectives: To investigate the presence of inactivating mutations in the FGF9 and FGFR2 gene in patients with 46,XY DSD by gonadal abnormalities. Casuistic and Methods: Thirty-three patients with 46,XY gonadal dysgenesis, 11 with the full form and 22 with the partial form. The coding regions of FGF9 and FGFR2 genes of all patients were amplified and sequenced. Investigations on the presence of deletions were made using the MLPA technique (\"Multiplex ligation-dependent probe amplification\"). Results: Mutations or deletions in the FGF9 gene were not found in any of the patients studied, only a few polymorphisms previously described. FGFR2 gene deletions were not found. A new non-synonymous variant in heterozygosis, c.1358 C> T (p.Ser453Leu) located in exon 10 of FGFR2 was found in two sisters with 46,XY partial gonadal dysgenesis. The mother is a carrier of the variant allele and the study of 147 control subjects did not identify the presence of this variant. The analysis of the variant on prediction sites, \"PolyPhen\", \"SIFT\" and \"Mutation Taster\" indicated that the new FGFR2 protein is possibly damaged. Conclusions: If the results of the prediction sites are confirmed by future functional studies the participation of the FGFR2 gene in human male gonadal determination will be proven

Os distúrbios do desenvolvimento sexual (DDS) 46,XY por anormalidades do desenvolvimento gonadal são doenças genéticas heterogêneas. Os testes genéticos que utilizam o sequenciamento de genes candidatos pelo método de Sanger é efetivo para o diagnóstico etiológico em menos de 40% desses pacientes. O sequenciamento de nova geração é uma ferramenta eficaz no diagnóstico de pacientes com DDSs. No presente estudo, utilizamos o sequenciamento exômico paralelo em larga escala (SEPLE) para identificar variantes alélicas potencialmente causadoras dos DDSs. Pacientes com síndrome de regressão testicular embrionária (SRTE) familial, membros de duas famílias brasileiras não relacionadas (família 1: dois irmãos afetados e pais não afetados e família 2: indivíduo índice, irmã não afetada e sobrinho afetado, filho da irmã do índice) foram selecionados inicialmente. Estes pacientes apresentavam micropenis, testículos ausentes ou disgenéticos e ausência de útero. O DNA genômico foi extraído de leucócitos de sangue periférico e o SEPLE foi realizado usando a plataforma Illumina-HiSeq-2500. Uma nova variante em heterozigose, c.923C > T, (p.Arg308Gln), no DHX37 foi identificada em todos os membros afetados das duas famílias brasileiras. O sequenciamento por Sanger confirmou a presença da variante em todos os afetados, no pai não afetado da F1 e na mãe não afetada do F2. A presença de efeito fundador da variante nestas duas famílias foi excluído, através da análise de 29 marcadores localizados no cromossomo 12q. Trinta e cinco pacientes com 46, XY DDS por anormalidades do desenvolvimento gonadal (6 com SRTE e 29 com disgenesia gonadal) esporádicos foram incluídos na pesquisa de variantes no DHX37 por Sanger ou por painel de genes candidatos (Plataforma Illumina-HiSeq-2500). As variantes c.923C > T, (p.Arg308Gln) em heterozigose e a variante c.451G > A, (p.Arg151Trp) em homozigose foram identificadas no DHX37 em dois pacientes com SRTE esporádicos. As variantes c.142C > T (p.Ala48Thr) e c.2020G > A (p.Arg674Trp) foram identificadas em heterozigose em dois pacientes esporádicos com disgenesia gonadal (DG). De acordo com o American College of Medical Genetics e Genomics guideline (ACMG), as variantes foram classificadas como provavelmente patogênicas (p.Arg308Gln e p.Arg674Trp), variante de significância clínica incerta (p.Arg151Trp) e variante benigna (p.Ala48Thr). Três variantes identificadas no DHX37 eram causadoras de doença em mais de três das ferramentas de previsão in silico utilizadas. Nenhuma das novas variantes no DHX37 foi encontrada nas bases de dados da população disponíveis (EXAC, 1000GENOME, ESP6500, gnomAD e abraOM) com uma frequência maior do que 0,01%. O padrão de metilação da região promotora do DHX37 dos membros afetados e não afetados das famílias 1 e 2 e controles femininos e masculino foi analisado utilizando o ensaio Infinium Methylation EPIC BeadChip (Illumina). Um sítio CpG hipometilado na região promotora do DHX37 foi observado apenas no pai da F1 quando comparado com as amostras dos filhos afetados, membros da F2 e controles. A análise imuno-histoquímica do padrão de expressão da proteína DHX37 foi realizada em amostras de testículos de oito indivíduos com diferentes idades cronológicas. Esta analise revelou que no tecido testicular de recém-nascidos, indivíduos em idade puberal e adultos, o DHX37 estava expresso em células germinativas em diferentes estágios de maturação (presentes nas espermatogonias, espermatócitos e espermátides e ausente nos espermatozoides). Este achado sugere que a proteína DHX37 pode ter um papel no processo de desenvolvimento das células germinativas. O DHX37 (12q24.31) codifica uma proteína DEAH (Asp-Glu-Ala-His) que pertence às famílias RNA helicases cujos membros estão envolvidos em quase todos os processos relacionados ao RNA, bem como ao controle do crescimento, proliferação e processos de diferenciação celular. Pacientes descritos com deleções na região 12q24.31, que contém o DHX37, apresentavam características sindrômicas e anormalidades genitais, como hipospadias ou micropenis. A presença de anormalidades genitais nestes pacientes reforça a hipótese de que o DHX37 está envolvido na etiologia dos DDSs 46,XY. Em conclusão, identificamos fortes evidências de um novo gene, o DHX37, envolvido no processo de desenvolvimento e manutenção das gônadas masculinas. Estudos complementares serão necessários para esclarecer o papel exato do DHX37 nas redes reguladoras de genes que controlam o desenvolvimento sexual humano / 46,XY disorders of sex development (DSD) associated with abnormalities of gonadal development are heterogeneous genetic diseases. Genetics testing using Sanger sequencing of candidate genes is effective for diagnosis in less than 40% of these patients. Next-generation sequencing has been a powerful genetic diagnostic tool in the investigation of DSD patients. In the present study, we used the whole exome sequencing (WES) to identify potentially DSD-causing allelic variants. Patients with familial embryonic testicular regression syndrome (ETRS) of two non-related Brazilian families (Family 1 (F1)- two affected brothers and the unaffected parents; Family 2 (F2)- index patient, his unaffected sister and an affected nephew, the son of the index\'s sister) were initially selected. The patients had micropenis, absent or dysgenetic testes and no uterus. Genomic DNA was extracted from peripheral blood leucocytes and WES was performed using the Illumina-HiSeq-2500 platform. A novel heterozygous variant, c.923C > T, (p.Arg308Gln), in the DHX37 gene was identified in all affected members of the two Brazilian families and in F1\'s father. Sanger sequencing confirmed the presence of the variant in the all of the affected members and in F1\'s father and in F2\'s mother. The presence of a founder effect in these families was investigated using 29 markers located on chromosome 12q and was ruled out. Thirty-five additional patients with sporadic 46,XY DSD associated with abnormalities of gonadal development (6 with ETRS and 29 with gonadal dysgenesis) were screened for variants in this novel candidate gene using Sanger or NGS-based targeted sequencing panel of DSD candidate genes (Illumina-HiSeq-2500 platform). The heterozygous variant c.923C > T (p.Arg308Gln) and the homozygous variant c.451G>A, (p.Arg151Trp) in the DHX37 were identified in two sporadic SRTE patients. The heterozygous variants c.142C > T (p.Ala48Thr) and c.2020G > A (p.Arg674Trp) were identified in two sporadic 46,XY gonadal dysgenesis (GD) patients. According to the American College of Medical Genetics and Genomics guidelines (ACMG) the variants were classified as likely pathogenic (p.Arg308Gln, p.Arg674Trp), variant of uncertain clinical significance (p.Arg151Trp and) and benign variant (p.Ala48Thr); and all three of them were disease causing in more than three of the in silico prediction tools used. None of the novel DHX37 variants identified were found in the available population databases (EXAC, 1000GENOME, ESP6500, gnomAD and abraOM) in more than 0.01%. Segregation analysis of DHX37 allelic variants was performed in 5 families and resulted in the autosomal dominant with incomplete penetrance and recessive inheritance patterns. DNA methylation pattern of the DHX37 promotor region of F1 and F2\'s affected and unaffected members and gender-matched controls was analyzed using the Infinium Methylation EPIC BeadChip (Illumina). One hypomethylated CpG site in the promoter region of the DHX37 was only observed in F1\'s father compared with the affected siblings, F2\'s members and controls. Immunohistochemical analysis of DHX37 protein expression pattern was performed on testis samples of eight individuals with different chronological ages. This analysis revealed that in the testicular tissue of newborns, pubertal and adults, the DHX37 was expressed in different stages of germ cells maturation (present in spermatogonia, spermatocytes and spermatids and absent in spermatozoa). This finding suggests that DHX37 protein might have a role in the process of germ-cells development. The DHX37 (12q24.31) encodes a DEAH (AspGlu- Ala-His) protein of the RNA helicase families, whose members are involved in almost all RNA-related process such as the control of cell growth, proliferation and differentiation processes. Previously described patients with 12q 24.31 deletions, which contains DHX37, showed syndromic features and genital abnormalities as hypospadias or micropenis. This phenotype reinforces the hypothesis that DHX37 is involved in the etiology of disorders in male sex development. In conclusion, a novel gene, the DHX37, involved in the process of development and maintenance of male gonads was identified. Further studies will be necessary to clarify the exact role of the DHX37 in the gene regulatory networks controlling human sex development

Gegenstand der Arbeit ist die Untersuchung der spezifischen Wärme von Holmium und YNi2B2C in den Temperaturbereichen von 50 bis 200 K bzw. von 380 mK bis 20 K in Magnetfeldern bis 9 T. In der vorliegenden Arbeit werden das kritische Verhalten von YNi2B2C und Eigenschaften des supraleitenden Zustands des nichtmagnetischen Seltenerd-Nickel-Borkarbids YNi2B2C mit Hilfe eines selbstentwickelten Messaufbaus der spezifischen Wärme nach der quasiadiabatischen Heizpulsmethode sowie von Holmium mit Hilfe der Relaxationsmethode untersucht. In dieser Arbeit konnten zuverlässige Aussagen über die kritischen Exponenten an einkristallinem Holmium gemacht werden. Die Untersuchung an Holmium beweist, dass das kritischen Verhalten der spezifischen Wärme nicht im Rahmen der Vorhersagen der chiralen Universalitätsklassen beschrieben werden kann. Anhand von Messungen der spezifischen Wärme konnte in dieser Arbeit bestätigt werden, dass YNi2B2C ein Multibandsupraleiter ist. Die positive Krümmung der Grenzlinie unterhalb Tc im Phasendiagramm liefert einen ersten Hinweis auf den Mehrband-Charakter von YNi2B2C. Im Nullfeld kann die elektronische spezifische Wärme im supraleitenden Zustand, ces(T), nicht im Rahmen der reinen BCS-Theorie erklärt werden. Bei tiefen Temperaturen konnte ein Restbeitrag durch normalleitende Elektronen nachgewiesen werden, der auf eine nicht vollständig geöffnete Energielücke hinweist. Eine mögliche Erklärung wäre, dass ein Band (oder mehrere Bänder) mit geringer Ladungsträgerkonzentration nicht zur Supraleitung beitragen. Dieses Ergebnis deckt sich mit de Haas-van Alphen-Messungen an isostrukturellen supraleitenden LuNi2B2C-Einkristallen, welche den Mehrband-Charakter der Supraleitung sowie eine verschwindende Energielücke in einem Band nahe legen. Das Fluktuationsverhalten der spezifischen Wärme von YNi2B2C in der Nähe des supraleitend-normalleitenden Übergangs stimmt gut mit demjenigen des 3D-XY-Modells überein.