No description available.

Takotsubo cardiomyopathy (TTC) is a disease characterized by transient left ventricular (LV) dysfunction and typical wall motion abnormalities in apical parts, without obvious signs of coronary influence. Due to its elusive natural cause and the lack of clarified pathology, further studies are needed. Thirteen patients presented with an episode of TTC, and referred to Örebro University Hospital (USÖ), were prospectively included and investigated by comparisons made at onset (acute phase) against at follow-up three months later (recovery phase). Including echocardiographic measurements, focused on biventricular systolic long-axis function and conventional diastolic function (DF) variables. Systolic improvement was shown, while most DF data were unchanged, suggesting that TTC is mainly a systolic disease affecting both ventricles. Diagnosis should include multidisciplinary engagement, as TTC associates both with emotional stress and pathological markers of physiological stress. In this thesis, such approach was offered to the aforementioned patients; to see if a common denominator could be found, thus, contributing to better handling. Emotional state was assessed, along with an array of cardiac investigations in addition to echocardiography. Acutely, imbalance in the autonomic cardiac control was shown, as well as a trend toward posttraumatic stress, but specific findings allowing conclusions on differential diagnosis could not be demonstrated. By adding another 15 TTC patients (i.e. 28 in total), through collaboration with observers from USA, a retrospective echocardiographic analysis could be done to further study DF; concluding that TTC associates with impairment of conventional DF variables which tends to parallel the systolic recovery, in contrary to the initial result but in line with other causesof LV dysfunction. Magnetic resonance imaging (MRI) is another method of choice at TTC. The USÖ patients had cardiac MRI, thus, a retrospective analysis was done to investigate the effect on LV geometry, both echocardiographic and by MRI; suggesting that TTC is consistently associated with increased LV mass, due to a local impact that seems to follow the change in LVconcentric wall motion.

Context:Broken heart syndrome or Takotsubo cardiomyopathy (TC) is a disorder characterized by transient left ventricular apical ballooning that almost invariably precedes emotional or physical stress. Although the patients with chronic kidney disease on hemodialysis have shown to exhibit sustained activity of sympathetic nervous system, the presentation of TC in these patients is a rare entity with few case reports in the literature. Case Report: A 75-year-old female with past medical history of end-stage renal disease presented with chest pressure and heaviness that started during her maintenance hemodialysis session. Electrocardiogram showed ST elevation and T wave inversion in V3-V6 leads. Emergent left heart catheterization was done that showed normal coronaries and akinesis of apical left ventricle wall consistent with TC. She was started on maximal medical management and underwent hemodialysis the next day without recurrence of the symptoms. Conclusion: TC may an underdiagnosed entity in patients on hemodialysis. However, it should be considered in the differential diagnosis in hemodialysis patients, particularly who presents with chest pain and/or symptoms.

No description available.

Developmental biology adresses how cells are organised into functional structures and eventually into a whole organism. It is crucial to understand the molecular basis for processes in development, by studying the expression and function of relevant genes and their relationship to each other. A gene function can be studied be creating loss-of-function situations, in which the change in developmental processes is examined in the absense of a functional gene product, or in gain-of-function studies, where a gene product is either intrinsically overproduced or ectopically upregulated. One approach for a loss-of-function situation is the creation of specific mutants in single genes, and the zebrafish (Danio rerio) has proven to be an excellent model organism for this purpose. In this thesis, I report on two forward genetic screens performed to find new mutants affecting brain development, in particular mutants defective in development and function of the midbrain-hindbrain boundary (MHB), an organiser region that patterns the adjacent brain regions of the midbrain and the hindbrain. In the first screen, I could identify 10 specific mutants based on morphology and the analysis of the expression patterns of lim1 and fgf8, genes functioning as early neuronal markers and as a patterning gene, respectively. Three of these mutants lacked an MHB, and by complementation studies, I identified these mutants as being defective in the spg locus. The second screen produced 35 new mutants by screening morphologically and with antibodies against acetylated Tubulin, which marks all axonal scaffolds, and anti-Opsin, which is a marker for photoreceptors in the pineal gland. According to their phenotype, I distributed the mutant lines into 4 phenotypic subgroups, of which the brain morphology group with 18 mutant lines was studied most intensively. In the last part of my thesis, I characterise one of these brain morphology mutants, broken heart. This mutant is defective in axonal outgrowth and locomotion, and shows a striking reduction of serotonergic neurons in the epiphysis and in the raphe nuclei in the hindbrain, structures involved in serotonin and melatonin production. Studies in other model organisms suggested a role of factors from the floor plate and the MHB in induction of the serotonergic neurons in the hindbrain, and using broken heart, I show that Fgf molecules such as Fgf4 and Fgf8 can restore partially the loss of serotonergic neurons in the mutant. I conclude that forward genetic screens are an invaluable tool to generate a pool of mutations in specific genes, which can be used to dissect complex processes in development such as brain development.

Developmental biology adresses how cells are organised into functional structures and eventually into a whole organism. It is crucial to understand the molecular basis for processes in development, by studying the expression and function of relevant genes and their relationship to each other. A gene function can be studied be creating loss-of-function situations, in which the change in developmental processes is examined in the absense of a functional gene product, or in gain-of-function studies, where a gene product is either intrinsically overproduced or ectopically upregulated. One approach for a loss-of-function situation is the creation of specific mutants in single genes, and the zebrafish (Danio rerio) has proven to be an excellent model organism for this purpose. In this thesis, I report on two forward genetic screens performed to find new mutants affecting brain development, in particular mutants defective in development and function of the midbrain-hindbrain boundary (MHB), an organiser region that patterns the adjacent brain regions of the midbrain and the hindbrain. In the first screen, I could identify 10 specific mutants based on morphology and the analysis of the expression patterns of lim1 and fgf8, genes functioning as early neuronal markers and as a patterning gene, respectively. Three of these mutants lacked an MHB, and by complementation studies, I identified these mutants as being defective in the spg locus. The second screen produced 35 new mutants by screening morphologically and with antibodies against acetylated Tubulin, which marks all axonal scaffolds, and anti-Opsin, which is a marker for photoreceptors in the pineal gland. According to their phenotype, I distributed the mutant lines into 4 phenotypic subgroups, of which the brain morphology group with 18 mutant lines was studied most intensively. In the last part of my thesis, I characterise one of these brain morphology mutants, broken heart. This mutant is defective in axonal outgrowth and locomotion, and shows a striking reduction of serotonergic neurons in the epiphysis and in the raphe nuclei in the hindbrain, structures involved in serotonin and melatonin production. Studies in other model organisms suggested a role of factors from the floor plate and the MHB in induction of the serotonergic neurons in the hindbrain, and using broken heart, I show that Fgf molecules such as Fgf4 and Fgf8 can restore partially the loss of serotonergic neurons in the mutant. I conclude that forward genetic screens are an invaluable tool to generate a pool of mutations in specific genes, which can be used to dissect complex processes in development such as brain development.

Made available in DSpace on 2016-04-28T20:39:48Z (GMT). No. of bitstreams: 1 Cristiane Corsini Prizanteli.pdf: 286050 bytes, checksum: 9c7474a7842e631bc56bc8c1f4c4f72c (MD5) Previous issue date: 2008-06-10 / Loss resulting from death is a critical situation, and the death of a spouse often represents one of the greatest losses in life. There is an increased risk of mortality among patients in grief, when compared to those not thrown into mourning, besides an increased use of health services. There have been investigations on individual and/or situational variables which might explain why a significant proportion of people in grief resulting from the death of a spouse have their health affected. Stress seems to be associated to a kind of cardiopathy called Broken Heart Syndrome. Such Syndrome may be considered as metaphor, which take place immediately after a severe physical or psychological stressful episode, to which an individual responds much the same way as to a heart attack. The aim of the present study was to figure out how mourning affected widowhood with presentation cardiac symptoms without physical causes. The study was conducted one year and five months after the death of her spouse. Our results indicated that the widow sustained severe psychological pain, which triggered the cardiac symptoms characterized as the Broken Heart Syndrome. Such severe psychological suffering leads to chest pain that is similar to a heart attack. The subject reported that her health care professionals did not sympathize with her psychological suffering. Furthermore, it was clear that the loss brought about consequences that can be seem in the whole family / A perda por morte é considerada situação de crise e a morte do cônjuge uma das perdas mais significativas da vida. Há aumento no risco de mortalidade em pacientes enlutados, quando comparados a indivíduos não enlutados, além de aumento na utilização dos serviços de saúde. Tem-se investigado variáveis individuais e/ou situacionais que expliquem por que proporção significativa de pessoas enlutadas pela perda do cônjuge têm a saúde afetada. O estresse parece estar associado a um tipo de cardiopatia denominado Síndrome do Coração Partido. Essa Síndrome pode ser considerada como metáfora que tem precedência imediata após um episódio de estresse físico ou psicológico intenso, que pode propiciar ao indivíduo reação semelhante à de um ataque cardíaco. O objetivo do estudo foi compreender o processo do luto por viuvez com apresentação de sintomas cardíacos sem causa orgânica. A pesquisa foi realizada um ano e cinco meses após a morte do cônjuge. Os resultados indicaram que a viúva mostrou dor psicológica intensa, desencadeando sintomas cardíacos caracterizados como Síndrome do Coração Partido. O sofrimento psicológico intenso leva à dor no peito que se assemelha a ataque cardíaco. A participante relata não ter encontrado acolhimento nos profissionais de saúde com relação à sua dor psíquica. Além disso, foi possível observar que a perda trouxe desdobramentos que aparecem em todo o grupo familiar

‘The Ophelia Versions: Representations of a Dramatic Type from 1600-1633’ interrogates early modern drama’s use of the Ophelia type, which is defined in reference to Hamlet’s Ophelia and the behavioural patterns she exhibits: abandonment, derangement and suicide. Chapter one investigates Shakespeare’s Ophelia in Hamlet, finding that Ophelia is strongly identified with the ballad corpus. I argue that the popular ballad medium that Shakespeare imports into the play via Ophelia is a subversive force that contends with and destabilizes the linear trajectory of Hamlet’s revenge tragedy narrative. The alternative space of Ophelia’s ballad narrative is, however, shut down by her suicide which, I argue, is influenced by the models of classical theatre. This ending conspires with the repressive legal and social restrictions placed upon early modern unmarried women and sets up a dangerous precedent by killing off the unassimilated abandoned woman. Chapter two argues that Shakespeare and Fletcher’s The Two Noble Kinsmen amplifies Ophelia’s folk and ballad associations in their portrayal of the Jailer’s Daughter. Her comedic marital ending is enabled by a collaborative, communal, folk-cure. The play nevertheless registers a proto-feminist awareness of the peculiar losses suffered by early modern women in marriage and this knowledge deeply troubles the Jailer’s Daughter’s happy ending. Chapter three explores the role of Lucibella in The Tragedy of Hoffman arguing that the play is a direct response to Hamlet’s treatment of revenge and that Lucibella is caught up in an authorial project of disambiguation which attempts to return the revenge plot to its morality roots. Chapters four and five explore the narratives of Aspatia in The Maid’s Tragedy and Penthea in The Broken Heart, finding in their very conformism to the behaviours prescribed for them, both by the Ophelia type itself and by early modern society in general, a radical protest against the limitations and repressions of those roles. This thesis is consistently invested in the competing dialectics and authorities of oral and textual mediums in these plays. The Ophelia type, perhaps because of Hamlet’s Ophelia’s identification with the ballad corpus, proves an interesting gauge of each play’s engagement with emergent notions of textual authority in the early modern period.