Revision of thesis--University of Illinois, Urbana, 1980. / Bibliogr. p. 217-226. Notes. Index.

Texte remanié de: Habili.-schr.--Berlin--Technische Universität, 1994. / Bibliogr. p. 611-639 Index.

Dissertação (mestrado)—Universidade de Brasília, Faculdade de Ciências da Saúde, Programa de Pós-Graduação em Ciências da Saúde, 2011. / Submitted by Alaíde Gonçalves dos Santos (alaide@unb.br) on 2012-06-06T13:50:59Z No. of bitstreams: 1 2011_MarianiCarlaPrudenteBatista.pdf: 2376937 bytes, checksum: 7fb074f870b25dd1772145cb9a2403b8 (MD5) / Approved for entry into archive by Jaqueline Ferreira de Souza(jaquefs.braz@gmail.com) on 2012-06-14T14:36:13Z (GMT) No. of bitstreams: 1 2011_MarianiCarlaPrudenteBatista.pdf: 2376937 bytes, checksum: 7fb074f870b25dd1772145cb9a2403b8 (MD5) / Made available in DSpace on 2012-06-14T14:36:13Z (GMT). No. of bitstreams: 1 2011_MarianiCarlaPrudenteBatista.pdf: 2376937 bytes, checksum: 7fb074f870b25dd1772145cb9a2403b8 (MD5) / Síndrome dos Ovários Policísticos (SOP) é um distúrbio endócrino complexo, de etiologia multifatorial, comum nas mulheres em fase reprodutiva, considerada a principal causa de infertilidade anovulatória, distúrbios menstruais e hiperandrogenismo nessa população. Dados atuais suportam que a SOP pode aumentar o risco para o desenvolvimento de diabetes mellitus tipo 2, dislipidemia, doenças cardiovasculares e carcinoma endometrial, enfatizando a necessidade de diagnóstico precoce da síndrome. Embora ainda não completamente elucidados, seus mecanismos moleculares e celulares envolvem anormalidades intrínsecas na esteroidogênese ovariana e adrenal, sugerindo um defeito esteroidogênico primário. Anormalidades neuroendócrinas parecem estar envolvidas na sua etiopatogenia, representadas principalmente pela pulsatilidade excessiva do LH, com aumento na amplitude dos seus pulsos, resultado de um aumento da sensibilidade da hipófise à estimulação GnRH. A base genética da SOP é desconhecida. Reporta-se significativa agregação familiar, entretanto, a determinação do seu modo de herança é difícil, uma vez que a apresentação clínica é muito heterogênea. Vários genes candidatos já foram avaliados com foco, recentemente, naqueles que codificam as enzimas esteroidogênicas na via de biossíntese de andrógenos e os envolvidos na secreção e ação da insulina. Considerando a repercussão funcional de variantes da subunidade beta específica do LH na fisiopatogenia de disfunções reprodutivas, o estudo ampliado da freqüência dos polimorfismos do gene LHB deve ajudar a esclarecer a heterogeneidade de suas manifestações clínicas, particularmente aquelas relacionadas à hiperandrogenemia. Estudamos assim a prevalência desses polimorfismos em controles (n=85) e casos de SOP (n=130) e sua associação com parâmetros clínicos e laboratoriais da síndrome. Através de seqüenciamento genético detectamos 11 polimorfismos na região codante do LHB, sendo 1 deles (233C>A/Thr78Asn) ainda não descrito na literatura. Na análise de associação entre a detecção destes polimorfismos e a presença de SOP, o poder estatístico consequente ao tamanho de nossas amostras não permitiu a observação de associações estatisticamente significativas, mas o nível de associação entre a presença do novo polimorfismo descoberto (233C>A/Thr78Asn) com a presença de SOP revelou um OR= 3,96 (95% IC= 0,43-189,12), sugerindo uma ligação a ser mais explorada em amostras maiores. A distribuição dos parâmetros clínicos estudados ficaram dentro dos níveis reportados na literatura. Observamos, entretanto, que dois polimorfismos, que segregam em desequilíbrio de ligação, são significativamente mais prevalentes na presença da hiperandrogenemia: rs1800447/rs34349826 (Trp28Arg/Ile35Thr) (p=0,015) e outros 2 parecem proteger contra hirsutismo severo embora estas associações não tenham apresentado resultados estatisticamente significativos em nível de p<0,05, mas de p<0,01: rs6521 (Val38=) (p=0,094) e 233C>A (p=0,063). Os resultados do nosso estudo corroboram outros recentemente publicados na literatura em que não foi possível demonstrar um papel causal para os polimorfismos conhecidos do gene LHB no desenvolvimento da SOP. Revelamos, no entanto, que o novo polimorfismo detectado (233C>A) deve ser objeto de mais investigações. ______________________________________________________________________________ ABSTRACT / Polycystic Ovary Syndrome (PCOS) is a complex endocrine disorder, of multifactorial a etiology, common in women of reproductive age and considered the leading cause of anovulatory infertility, menstrual disorders, and hyperandrogenism in this population. PCOS is also a risk factor for the development of type 2 diabetes mellitus, dyslipidemia, cardiovascular disease, and endometrial carcinoma, which emphasizes the need for early diagnosis of the syndrome. Although not yet fully understood, its molecular and cellular mechanisms involve intrinsic ovarian and adrenal steroidogenesis abnormalities, suggesting these to be a primary defect. It appears that there are also accompanying neuroendocrine abnormalities along the natural history of PCOS, represented mainly by excessive luteinizing hormone (LH) pulsatility, with the amplified pulse amplitude resulting from increased sensitivity of the pituitary gland to GnRH stimulation. The genetic basis of PCOS is still largely unknown despite significant family clustering; determining its mode of inheritance is particularly difficult given the wide variability in clinical presentation. Several candidate genes have been evaluated with focus switching recently to genes that encode steroidogenic enzymes that regulate androgen biosynthesis and those involved in insulin secretion and action. The crucial functional role played by specific LH beta (LHB) subunits in various reproductive disorders makes these units natural candidates for elucidating the causal pathway and the many clinical manifestations of PCOS, particularly those related to hyperandrogenemia. The present project is a study of the prevalence of these polymorphisms in 85 controls and 130 PCOS cases and their association with clinical and laboratory parameters of the syndrome. Through genetic sequencing 11 polymorphisms were detected in the coding region of LHB, one of them, 233C>A/Thr78Asn, not yet described in the literature. No statistically significant associations were found between polymorphisms and the presence of PCOS, probably due to small sample size and consequent lack of statistical power, however, the level of association between detection of the newly discovered polymorphism (233C>A) and PCOS revealed an OR=3.96 (95% CI = 0.43-189.12), suggesting a possible connection to be further explored in larger samples. The distribution of the clinical parameters studied matched those already reported in the literature. Notable exceptions included two polymorphisms that secrete in link imbalance and were found to be significantly more prevalent in the presence of hyperandrogenemia: rs1800447/rs34349826 (Trp28Arg/Ile35Thr) (p=0.015) and two other which seemed to be protective against severe hirsutism. The latter however, were not found to be statistically significant at the level of p<0,05, but instead, at the level of p<0,01: rs6521 (Val38=) (p=0,094) e 233C>A (p=0,063). The results of this study corroborate other recently published in the literature in that it was not possible to demonstrate a causal role for the known LHB gene polymorphisms in PCOS. However, a newly detected polymorphism (233C>A) should probably be the object of further investigation.

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This paper is about Edith Steins phenomenological investigation on empathy, based on the dissertation she wrote for Edmund Husserl: Zum Problem der Einfühlung. The philosophical method she used was an early phenomenological realism, practiced by phenomenologists in prewar-time, and she was an active member of the Göttingen philosophical society founded in 1907. Her analysis of the phenomenon empathy also includes a theory of emotions which recently has been brought up in the empathy-debate as crucial to an understanding of our empathic experience and our basic intersubjective experience. By looking in to how we perceive the others emotions Stein includes a survey, in the analysis of empathy, over different layers of our personality: from the outer bodily dimension to the inner core in the psychophysical individual. She provides for a phenomenological insight into the structures and layers of the other person, which then creates an understanding of how the emotional aspect of the empathic act discloses the others personality and values. / Den här uppsatsen handlar om Edith Steins fenomenologiska analys av empati-begreppet, med grund i doktorsavhandlingen hon skrev för Husserl: Zum Problem der Einfühlung. Hon ägnade sig åt en realistisk fenomenologi i likhet med samtida fenomenologer och var med i Göttingen filosofiska sällskap (grundat 1907). I Steins (tidiga) filosofi får vi dessutom en fenomenologisk inblick i de underliggande strukturerna i psyket, samt en teori om känslor som visar på hur kroppen och psyket i en sammanhängande enhet ger uttryck för våra upplevelser. Uppsatsen lyfter, tillsammans med ny forskning, fram den tyska innebörden av ordet empati (Einfühlung), där Stein på ett realistiskt vis beskriver det kännande jaget som fenomen - det empiriska jaget. Ordet översatt till svenska blir inkännande och det är denna innebörd som här specifikt betraktats i samband med den empatiska akten. Det handlar först och främst om den andres upplevelser och känslor som då utgör fokus i empati - där Steins undersökning av den empatiska upplevelsen och de olika känsloskikten i personen även bidrar till en förståelse för hur känslorna avslöjar personlighet och värden, i en grundläggande intersubjektiv upplevelse.

Thesis (M.A.)--Bowling Green State University, 2008. / Document formatted into pages; contains v, 93 p. Includes bibliographical references.

This dissertation consists of two parts. In the first part we show that for 1 k 1, a complex manifold M of dimension at least k in the boundary of a smooth bounded pseudoconvex domain in Cn is an obstruction to compactness of the @- Neumann operator on (p, q)-forms for 0 p k n, provided that at some point of M, the Levi form of b has the maximal possible rank n &#8722; 1 &#8722; dim(M) (i.e. the boundary is strictly pseudoconvex in the directions transverse to M). In particular, an analytic disc is an obstruction to compactness of the @-Neumann operator on (p, 1)-forms, provided that at some point of the disc, the Levi form has only one vanishing eigenvalue (i.e. the eigenvalue zero has multiplicity one). We also show that a boundary point where the Levi form has only one vanishing eigenvalue can be picked up by the plurisubharmonic hull of a set only via an analytic disc in the boundary. In the second part we obtain a weaker and quantified version of McNeal’s Property ( eP) which still implies the existence of a Stein neighborhood basis. Then we give some applications on domains in C2 with a defining function that is plurisubharmonic on the boundary.

Diss. Universität Düsseldorf. / Includes bibliographical references (p. 168-176) and indexes.

Zugl.: Diss.