Seiner excellence dem Herrn Geheimen Rathe und Ritter Baron von Nicolai bei dem Wechsel eines neuen Jahres: Wiburg d. I Januar 1819

Julkaisuvuosi nimekkeestä.

A cidade-jardim de Ebenezer Howard: um estudo de sua influência para a circulação de ideias e modelos no urbanismo do século XX

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior

La puesta en escena de la serie de comedias de magia "Cuando hay falta de hechiceros lo quieren ser los gallegos" y "Asombro de Salamanca" (1741-1775), de Nicolás González Martínez

Esta tesis comienza en el punto donde concluía el trabajo pionero sobre comedia de magia del XVIII emprendido por Joaquín Álvarez Barrientos. Planteaba él entonces la necesidad de saber más sobre los hombres y mujeres de la época para comprender mejor la comedia de magia como género escénico, con el objetivo de responder la pregunta que tantos dieciochistas nos hemos hecho: ¿por qué la comedia de magia tuvo tanto éxito? Mi investigación partió también de sus respuestas: se debió, sobre todo, a motivos ideológicos y espectaculares. Comprender la comedia de magia como género escénico quiere decir comprender todos los mecanismos de la materialidad de su puesta en escena y de la relación establecida entre espectáculo y espectadores. Implica comprender la teatralidad a un nivel que no es solo textual, sino físico y relacional. Las relaciones y reacciones que desataba la comedia de magia eran tremendamente pasionales y opuestas, como demuestran los datos de que disponemos: las espectaculares recaudaciones, de un lado, y las múltiples diatribas y prohibiciones, de otro. Así que, la siguiente pregunta que era necesario plantear era: ¿por qué molestaban tanto las comedias de magia? En el siglo XVIII ocurrió un acontecimiento especialmente traumático, el denominado «Motín contra Esquilache», que tuvo numerosas consecuencias para la sociedad en general pero, sobre todo, para el teatro. De hecho, una de las primeras medidas que el gobierno del conde de Aranda emprende nada más acabar con las revueltas es la Reforma del teatro. Haciendo un razonamiento inverso, surgía la hipótesis de que el teatro, en un sentido amplio, y en concreto la comedia de magia, hubiera tenido más intervención en el motín de lo que se piensa, tanto por sus temáticas, como por las posibilidades de encuentro y organización social que la asistencia al teatro propiciaba. Surgía pues, la necesidad de profundizar en la reconstrucción de una teoría estética de la comedia de magia, así como de estudiar el hecho teatral durante los años centrales del siglo, en concreto, desde la construcción de los nuevos coliseos, pues parecía probable que el cambio de espacio hubiera propiciado algún cambio de mentalidad…

Ihanteena orjuuteen perustuva kristillinen yhteiskunta – Uskonnollinen ja yhteiskunnallinen orjuuden ja etelävaltioiden puolustus baptistipastori Ebenezer W. Warrenin romaanissa Nellie Norton

Yhdysvalloissa kehittyi noin vuosina 1850–1865 erityinen orjuutta puolustamaan noussut kaunokirjallisuuden lajityyppi. Sen synty oli osa etelävaltioiden elämäntavan ja siihen keskeisesti liittyneen orjuuden taakse organisoitunutta puolustautumista, joka kehittyi erityisesti kolmena Yhdysvaltojen sisällissotaa edeltäneenä vuosikymmenenä, jolloin etelän orjajärjestelmä joutui kovan arvostelun kohteeksi. Orjuuden puolustajien kirjoittama romaanikirjallisuus voidaan nähdä eräänlaisena etelän vastareaktiona Harriet Beecher Stowen suuren suosion saaneelle orjuutta kritisoineelle romaanille Setä Tuomon tupa, joka julkaistiin vuonna 1852. Keskityn tutkielmassani yhteen tämän orjuutta puolustaneen romaanikirjallisuuden edustajaan, baptistipastori Ebenezer W. Warrenin vuonna 1864 julkaisemaan romaaniin Nellie Norton: or Southern Slavery and the Bible. A scriptural refutation of the principal arguments upon which the abolitionists rely. A vindication of southern slavery from the old and new testaments. Romaani sijoittuu julkaisuajankohtansa puolesta lajityyppinsä viimeisimpien edustajien joukkoon. Tutkielmassani tarkastellaan, minkälaisista argumenteista romaanin keinoin esitetty orjuuden puolustus koostuu. Tämän lisäksi tarkastelen myös sitä, millainen kuva romaanissa annetaan etelävaltioiden, ja toisaalta niiden vastapuolena näyttäytyvien pohjoisten osavaltioiden ja Englannin elämäntavasta ja maailmankuvasta. Tutkielmani osoittaa orjuuden puolustuksen rakentuvan Warrenin romaanissa erityisesti uskonnollisista, rasistisista sekä yhteiskunnallisista argumenteista. Romaanissa luodaan näiden kautta voimakas vastakkainasettelu etelän orjayhteiskunnan ja pohjoisen ja Englannin vapaaseen työvoimaan perustuneiden teollistuneiden yhteiskuntien välille. Etelän kirjaimelliset ja konservatiiviset tulkinnat Raamatusta ja sen asemasta moraalin ja yhteiskuntajärjestyksen ylimpänä määrittelijänä asetetaan abolitionistien harhaoppisiksi esitettyjen liberaalimpien ja modernimpien raamatuntulkintojen vastakohdaksi. Vastaavasti etelän orjuuteen perustuvan yhteiskunnan rakenteet ja instituutiot esitetään raamatullisina ja hyveellisinä, siinä missä vapaaseen työvoimaan perustuneet yhteiskunnat esitetään moraalittomina ja raadollisina. Romaanista välittyy erityisesti kuva konservatiivisesta maailmasta, jossa uskonnolliset ja rasistiset ajattelumallit ovat keskeisessä asemassa pyrittäessä puolustamaan ja ylläpitämään orjuuteen perustuvaa eteläistä elämäntapaa.

A cidade-jardim de Ebenezer Howard: um estudo de sua influência para a circulação de ideias e modelos no urbanismo do século XX

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior

Efeitos da secagem na qualidade fisiológica de sementes de cajuí (Anacardium giganteum W. Hancock ex Engl.).

Anacardium giganteum, conhecida como cajuí, é uma espécie nativa da Amazônia, que vem sendo explorada pelo setor madeireiro do Estado do Pará. O objetivo do trabalho foi avaliar o efeito da secagem sobre a qualidade fisiológica de sementes de cajuí. Foi determinado o teor de água das sementes e sua viabilidade através do teste de germinação. Foram quantificados o número de dias para iniciar a emergência, o índice de velocidade de emergência, emergência, germinação, plântulas anormais e sementes mortas. O delineamento experimental foi inteiramente casualizado, com três tratamentos (teores de água de 35,6%, 21,4% e 16,6%) e quatro repetições de 25 sementes cada. Não houve diferença significativa na germinação das sementes com 35,6 e 21,4% de água, as quais apresentaram 89% e 77% de germinação, respectivamente. Entretanto, sementes com 16,6% de água, apresentaram redução na porcentagem de germinação (65%) e aumento na porcentagem de sementes mortas (33%). Sementes de A. giganteum são sensíveis a secagem e podem ser classificadas como intermediárias no armazenamento.

Management and organisational barriers in the acquisition of computer usage skills by mature age workers

Aim: To investigate workplace cultures in the acquisition of computer usage skills by mature age workers. Methods: Data were gathered through focus groups conducted at job network centres in the Greater Brisbane metropolitan region. Participants who took part were a mixture of workers and job-seekers. Results: The results suggest that mature age workers can be exposed to inappropriate computer training practices and age-insensitive attitudes towards those with low base computer skills. Conclusions: There is a need for managers to be observant of ageist attitudes in the work place and to develop age-sensitive strategies to help mature age workers learn computer usage skills. Mature age workers also need to develop skills in ways which are practical and meaningful to their work.

Levels of cardiac knowledge and cardiopulmonary resuscitation training among older people in Queensland

Objectives: The current study was conducted to determine levels of cardiac knowledge and cardiopulmonary resuscitation (CPR) training in older people in Queensland, Australia.---------- Methods: A telephone survey of 4490 Queensland adults examined respondents’ knowledge of coronary heart disease (CHD) risk factors, knowledge of heart attack symptoms, knowledge of the local emergency telephone number, as well as respondents’ rates and recency of training in CPR.---------- Results: Older participants, aged 60 years and over, were approximately one and a half times more likely than the 30–39 year-old reference group to have limited knowledge of heart disease risk factors (OR = 1.53), and low knowledge of heart attack symptoms (OR = 1.60). Knowledge of the local emergency telephone number also decreased with age. Older participants had significantly lower rates of training in CPR, with almost three quarters (71.7%) reporting that they had never been trained. Older people who had completed CPR training were significantly less likely to have done so recently.---------- Conclusions: Cardiac knowledge levels and CPR training rates in older Queensland persons were lower than those found in the younger population.

Older patients request more information : a survey of use of written patient education materials in general practice

Objectives: To determine GPs' reported use of written education materials with older patients and older patients' reported receipt of these materials. To determine GPs' and older patients' perceptions of written materials.---------- Method: Using self-report questionnaires, two populations were surveyed; a randomised sample of 50 GPs (29 males and 21 females) practising in Brisbane's southern suburbs and a convenience sample of 188 older community-dwelling people (aged over 64 years).----------- Results: All GPs reported using written materials with patients, although 28% had not given any to the Last 10 patients. This increased to 46% when patients were older. Twenty percent of patients wanted more written information from their GP, while some GPs believed that older patients preferred verbal information and gave out written information only when they perceived patient interest. All GPs reported giving written materials at the time of consultation and over two thirds discussed the content with patients. Just over 50% of patients reported receiving written information from GPs in the Last six months and only hall of these again discussed it directly with their GP. Overall, patients were more positive than GPs about the value of written education materials.---------- Conclusions: Older patients' desire for written information may be better met if they are more assertive in requesting this of GPs and GPs may better serve their patients' needs if they make written information more readily available to them. Better access to materials and more financial incentives to give them out might also increase GPs' use of written materials.

Poor functional health literacy : the silent disability for older people

In this information age, people are confronted by verbal, visual and written information. This is especially important in the health field, where information is needed to follow directions, understand prescriptions and undertake preventive behaviours. If provided in written form, much of this information may be inaccessible to people who cannot adequately read. Although poor literacy skills affect all groups in the population, older adults with fewer years of education seem to be particularly disadvantaged by an increasing reliance on written communication of health information. With older age comes a higher risk of illness and disability and a greater potential need to access the health system. As a result, poor literacy skills of older individuals may directly impact their health status. This paper explores the link between functional literacy and health, particularly for the older population, provides strategies to practitioners for the management of this problem, and suggests research initiatives in this area.

Biochemical characterization of Aprataxin, the protein deficient in Ataxia with Oculomotor Apraxia type 1

Neurodegenerative disorders are heterogenous in nature and include a range of ataxias with oculomotor apraxia, which are characterised by a wide variety of neurological and ophthalmological features. This family includes recessive and dominant disorders. A subfamily of autosomal recessive cerebellar ataxias are characterised by defects in the cellular response to DNA damage. These include the well characterised disorders Ataxia-Telangiectasia (A-T) and Ataxia-Telangiectasia Like Disorder (A-TLD) as well as the recently identified diseases Spinocerebellar ataxia with axonal neuropathy Type 1 (SCAN1), Ataxia with Oculomotor Apraxia Type 2 (AOA2), as well as the subject of this thesis, Ataxia with Oculomotor Apraxia Type 1 (AOA1). AOA1 is caused by mutations in the APTX gene, which is located at chromosomal locus 9p13. This gene codes for the 342 amino acid protein Aprataxin. Mutations in APTX cause destabilization of Aprataxin, thus AOA1 is a result of Aprataxin deficiency. Aprataxin has three functional domains, an N-terminal Forkhead Associated (FHA) phosphoprotein interaction domain, a central Histidine Triad (HIT) nucleotide hydrolase domain and a C-terminal C2H2 zinc finger. Aprataxins FHA domain has homology to FHA domain of the DNA repair protein 5’ polynucleotide kinase 3’ phosphatase (PNKP). PNKP interacts with a range of DNA repair proteins via its FHA domain and plays a critical role in processing damaged DNA termini. The presence of this domain with a nucleotide hydrolase domain and a DNA binding motif implicated that Aprataxin may be involved in DNA repair and that AOA1 may be caused by a DNA repair deficit. This was substantiated by the interaction of Aprataxin with proteins involved in the repair of both single and double strand DNA breaks (XRay Cross-Complementing 1, XRCC4 and Poly-ADP Ribose Polymerase-1) and the hypersensitivity of AOA1 patient cell lines to single and double strand break inducing agents. At the commencement of this study little was known about the in vitro and in vivo properties of Aprataxin. Initially this study focused on generation of recombinant Aprataxin proteins to facilitate examination of the in vitro properties of Aprataxin. Using recombinant Aprataxin proteins I found that Aprataxin binds to double stranded DNA. Consistent with a role for Aprataxin as a DNA repair enzyme, this binding is not sequence specific. I also report that the HIT domain of Aprataxin hydrolyses adenosine derivatives and interestingly found that this activity is competitively inhibited by DNA. This provided initial evidence that DNA binds to the HIT domain of Aprataxin. The interaction of DNA with the nucleotide hydrolase domain of Aprataxin provided initial evidence that Aprataxin may be a DNA-processing factor. Following these studies, Aprataxin was found to hydrolyse 5’adenylated DNA, which can be generated by unscheduled ligation at DNA breaks with non-standard termini. I found that cell extracts from AOA1 patients do not have DNA-adenylate hydrolase activity indicating that Aprataxin is the only DNA-adenylate hydrolase in mammalian cells. I further characterised this activity by examining the contribution of the zinc finger and FHA domains to DNA-adenylate hydrolysis by the HIT domain. I found that deletion of the zinc finger ablated the activity of the HIT domain against adenylated DNA, indicating that the zinc finger may be required for the formation of a stable enzyme-substrate complex. Deletion of the FHA domain stimulated DNA-adenylate hydrolysis, which indicated that the activity of the HIT domain may be regulated by the FHA domain. Given that the FHA domain is involved in protein-protein interactions I propose that the activity of Aprataxins HIT domain may be regulated by proteins which interact with its FHA domain. We examined this possibility by measuring the DNA-adenylate hydrolase activity of extracts from cells deficient for the Aprataxin-interacting DNA repair proteins XRCC1 and PARP-1. XRCC1 deficiency did not affect Aprataxin activity but I found that Aprataxin is destabilized in the absence of PARP-1, resulting in a deficiency of DNA-adenylate hydrolase activity in PARP-1 knockout cells. This implies a critical role for PARP-1 in the stabilization of Aprataxin. Conversely I found that PARP-1 is destabilized in the absence of Aprataxin. PARP-1 is a central player in a number of DNA repair mechanisms and this implies that not only do AOA1 cells lack Aprataxin, they may also have defects in PARP-1 dependant cellular functions. Based on this I identified a defect in a PARP-1 dependant DNA repair mechanism in AOA1 cells. Additionally, I identified elevated levels of oxidized DNA in AOA1 cells, which is indicative of a defect in Base Excision Repair (BER). I attribute this to the reduced level of the BER protein Apurinic Endonuclease 1 (APE1) I identified in Aprataxin deficient cells. This study has identified and characterised multiple DNA repair defects in AOA1 cells, indicating that Aprataxin deficiency has far-reaching cellular consequences. Consistent with the literature, I show that Aprataxin is a nuclear protein with nucleoplasmic and nucleolar distribution. Previous studies have shown that Aprataxin interacts with the nucleolar rRNA processing factor nucleolin and that AOA1 cells appear to have a mild defect in rRNA synthesis. Given the nucleolar localization of Aprataxin I examined the protein-protein interactions of Aprataxin and found that Aprataxin interacts with a number of rRNA transcription and processing factors. Based on this and the nucleolar localization of Aprataxin I proposed that Aprataxin may have an alternative role in the nucleolus. I therefore examined the transcriptional activity of Aprataxin deficient cells using nucleotide analogue incorporation. I found that AOA1 cells do not display a defect in basal levels of RNA synthesis, however they display defective transcriptional responses to DNA damage. In summary, this thesis demonstrates that Aprataxin is a DNA repair enzyme responsible for the repair of adenylated DNA termini and that it is required for stabilization of at least two other DNA repair proteins. Thus not only do AOA1 cells have no Aprataxin protein or activity, they have additional deficiencies in PolyADP Ribose Polymerase-1 and Apurinic Endonuclease 1 dependant DNA repair mechanisms. I additionally demonstrate DNA-damage inducible transcriptional defects in AOA1 cells, indicating that Aprataxin deficiency confers a broad range of cellular defects and highlighting the complexity of the cellular response to DNA damage and the multiple defects which result from Aprataxin deficiency. My detailed characterization of the cellular consequences of Aprataxin deficiency provides an important contribution to our understanding of interlinking DNA repair processes.