Inaug.-diss.--Giessen. / Lebenslauf.

莊如欣. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 778-789). / Abstracts in Chinese and English. / Zhuang Ruxin. / Chapter 第一章 --- 緒言 --- p.1 / Chapter 第一節 --- 馬端臨與《文獻通考´Ø經籍考》 --- p.1 / Chapter 第二節 --- 前人硏究槪述 --- p.2 / Chapter 第三節 --- 硏究動機及方法 --- p.7 / Chapter 第二章 --- 《經籍考》史部總論 --- p.11 / Chapter 第一節 --- 目錄分類的依據 --- p.11 / Chapter 第二節 --- 分類的特點 --- p.18 / Chapter 第二節 --- 目錄史上的價値 --- p.27 / Chapter 第三節 --- 小結 --- p.32 / Chapter 第三章 --- 分論一：正史類 --- p.33 / Chapter 第一節 --- 正史的定義 --- p.33 / Chapter 第二節 --- 正史與正統觀 --- p.38 / Chapter 第三節 --- 目錄分類的問題 --- p.44 / Chapter 第四節 --- 歸類的特點 --- p.47 / Chapter 第五節 --- 小結 --- p.51 / Chapter 第四章 --- 分論二 ：起居注類 --- p.53 / Chapter 第一節 --- 起居注與史官記注制度 --- p.53 / Chapter 第二節 --- 起居注、實錄、日曆、時政記的歸類 --- p.60 / Chapter 第三節 --- 分類背後的理念 --- p.64 / Chapter 第四節 --- 小結 --- p.70 / Chapter 第五章 --- 分論三：雜史類與傳記類 --- p.71 / Chapter 第一節 --- 雜史、傳記的內容性質 --- p.71 / Chapter 第二節 --- 類目設置與編次 --- p.81 / Chapter 第三節 --- 歸類的標準 --- p.83 / Chapter 第四節 --- 小結 --- p.94 / Chapter 第六章 --- 分論四:僞史霸史類 --- p.96 / Chapter 第一節 --- 僞史類與霸史類的交替出現 --- p.96 / Chapter 第二節 --- 書目的輯錄情況 --- p.98 / Chapter 第三節 --- 僞、霸觀與目錄分類 --- p.105 / Chapter 第四節 --- 僞史、霸史類的合倂 --- p.111 / Chapter 第五節 --- 互著隱含的歷史觀 --- p.114 / Chapter 第六節 --- 小結 --- p.123 / Chapter 第七章 --- 分論五：史評史鈔類 --- p.124 / Chapter 第一節 --- 史鈔、史評的定義 --- p.124 / Chapter 第二節 --- 史鈔、史評的獨立成類 --- p.128 / Chapter 第三節 --- 史鈔、史評與史學發展 --- p.132 / Chapter 第四節 --- 類目的設創 --- p.136 / Chapter 第五節 --- 書籍歸類的革新 --- p.141 / Chapter 第六節 --- 小結 --- p.148 / Chapter 第八章 --- 分論六：時令類 --- p.151 / Chapter 第一節 --- 時令類與農家類 --- p.151 / Chapter 第二節 --- 時令類書籍盛於唐、宋 --- p.157 / Chapter 第三節 --- 類目的歸屬 --- p.160 / Chapter 第四節 --- 類目的源流 --- p.161 / Chapter 第五節 --- 時令書籍的歸類 --- p.162 / Chapter 第六節 --- 小結 --- p.166 / Chapter 第九章 --- 結語 --- p.167 / 附錄凡例 --- p.171 / 附錄一正史類對照表 --- p.173 / 附錄二起居注類對照表 --- p.279 / 附錄三雜史類對照表 --- p.356 / 附錄四傳記類對照表 --- p.407 / 附錄五僞史霸史類對照表 --- p.641 / 附錄六史評史鈔類對照表 --- p.700 / 附錄七時令類對照表 --- p.755 / 參考書目 --- p.778

The second half of the thirteenth century is a rather obscure period in Spanish history. Only one fairly detailed Christian chronicle exists for the reign of each of the three kings that ruled during that time. Since these works were not composed until the middle of the following century, especially the earliest years which the author describes, the 1250's and 1260's, are full of anachronisms. The few other accounts that treat of the period are quite brief and of not much help. Alfonso el Sabio had until 1275 most extensive foriegn interests, and his plans have left many traces in the archives of other countries, especially of some of the city-states of Northern Italy. From these foreign accounts many obscure points in Alfonso's reign can be clarified, since it is precisely on the international plane where the Castilian chronicle of his reign fails. Taking Antonio Ballesteros y Beretta's work on the itinerary of Alfonso el Sabio as point of departure, the present essay tries to point out some of the shortcomings of Castilian fourteenth-century historiography. / Arts, Faculty of / Central Eastern Northern European Studies, Department of / Graduate

As bifenilas policloradas (PCBs) são um grupo de compostos hidrocarbonetos halogenados aromáticos, bioacumulativos em organismos vivos e persistente no ambiente. Além da atividade disruptora endócrina, os PCBs podem aumentar os níveis de espécies reativas de oxigênio (ROS), levando ao estresse oxidativo e alteração da metilação de DNA que são fatores importantes nas etiologias da hepatotoxicidade, infertilidade masculina e doença renal. Estes agentes tóxicos podem causar disfunção mitocondrial e distúrbios que afetam a produção de ATP, ROS e morte celular, ocasionando danos à saúde humana. O presente trabalho tem como objetivo investigar possíveis alterações genotóxicas e epigenéticas causadas pelo aroclor 1254 em fígado, rim e testículo, além de verificar a indução de estresse oxidativo e disrupção dos metabólitos intermediários do ciclo de Krebs nos referidos tecidos. Camundongos machos C57/BL6 foram expostos ao Aroclor 1254 em diferentes doses (5, 50, 500 e 1000 ug/kg) por gavagem, uma vez a cada três dias, durante 50 dias. Após a exposição, os animais foram eutanasiados, os órgãos coletados e espermatozoides obtidos a partir dos epidídimos. A peroxidação lipídica em plasma e tecidos foi avaliada pela quantificação de malonaldeído (MDA) por HPLC/DAD. Os níveis de intermediários da via glicolítica, do ciclo de Krebs, de alguns nucleotídeos e aminoácidos, marcas epigenéticas (5-mC e 5-hmC) e adutos de DNA (8-oxodG e CEdG) foram quantificados por HPLC-ESI-MS/MS. A abordagem de benchmark dose (BMD) foi utilizada para a modelagem dose resposta. Após exposição, não foram observadas diferenças significativas da variação da massa corporal, e a razão do peso testicular, fígado e rim por massa corporal. No tecido hepático, foi observado aumento da peroxidação lipídica. Houve redução significativa dos níveis de ATP, ADP, razão NADP+/NADPH, piruvato, malato, fumarato e glutamato. Observou-se redução significativa dos níveis de 5-mC e 5-hmC no DNA nuclear (nDNA), enquanto não foram observadas alterações dos níveis dos adutos. Em DNA mitocondrial (mtDNA) não foram observadas alterações nas marcas epigenéticas, no entanto foi obtido aumento significativo no aduto 8-oxodG após exposição ao Aroclor 1254. No tecido renal foi observado aumento significativo de MDA. Houve aumento significativo dos níveis de lactato e malato e reduções de ATP, ADP, glutamina, NAD+. Foi observada a hipohidroximetilação do mtDNA. As marcas 5-mC de mtDNA, 5mC de nDNA e adutos de DNA nuclear e mitocondrial não apresentaram diferenças após exposição a PCBs. Nos testículos foi verificada redução significativa dos níveis de glutamato, malato, succinato, fumarato e razão NADH/NAD+, hipohidroximetilção em mtDNA e hipermetilação em nDNA. Não foram observadas alterações de 5-mC em mtDNA e 5hmC em nDNA. Não foram verificadas alterações dos níveis de MDA e adutos em nDNA. Adicionando, foi observada redução dos níveis de 5-mC em DNA global de espermatozoide. Os limites inferiores do intervalo de confiança da BMD foram estimados para que estes marcadores possam ser usados na avaliação de riscos de PCBs. Os dados obtidos apontam o Aroclor 1254 como indutor de alterações do metabolismo intermediário, das marcas epigenéticas e estresse oxidativo. Essas alterações podem afetar vias celulares, levando à morte ou transformação, e aumentando o risco de doenças. / Polychlorinated biphenyls (PCBs) are a group of aromatic halogenated hydrocarbon compounds, which bioaccumulate in living organisms and is persistent in the environment. Besides their endocrine disrupting activity, PCBs may increase the levels of reactive oxygen species (ROS), leading to oxidative stress and alter DNA methylation that are important factors in the etiology of liver toxicity, male infertility, and kidney disease. These toxic agents can cause mitochondrial dysfunction and disorders that affect the production of ATP, ROS and cell death, thereby leading to health-related problems. The present work aimed at investigating possible genotoxic and epigenetic changes caused by aroclor 1254 in the liver, kidney and testis, as well as determine the induction of oxidative stress and disruption of intermediate metabolites in these tissues. Male C57/BL6 mice were exposed to Aroclor 1254 at different doses (5, 50, 500 and 1000 µg/kg) by gavage, once every three days, for 50 days. After the exposure period, the animals were euthanized, organs collected, and sperms obtained from the epididymis. Lipid peroxidation in plasma and tissues was determined by quantification of malonaldehyde (MDA) using HPLC/DAD. The levels of intermediate metabolites, epigenetic marks (5-mC and 5-hmC) and DNA adducts (8-oxodG and CEdG) were quantified by HPLC-ESI-MS/MS. The Benchmark dose approach (BMD) was used for dose response modeling. No significant differences in body weight variation, testicular, liver and kidney weight to body weight ratio were observed after exposure. However, in hepatic tissues, an increase in lipid peroxidation was observed. There were significant decreases in the intermediate metabolites including the levels of ATP, ADP, pyruvate, NADP+/NADPH ratio, malate and fumarate, as well as glutamate. Significant reduction of 5-mC and 5-hmC levels in nuclear DNA (nDNA) were observed, whereas no changes were observed in DNA adducts. The epigenetic marks in mitochondrial DNA (mtDNA) were not changed; however, a significant increase was observed in 8-oxodG adduct after exposure to Aroclor 1254. In renal tissues, data showed a significant increase in MDA, while for the intermediate metabolites, the levels of lactate and malate were significantly elevated, whereas significant reductions were recorded for ATP, ADP, glutamine, and NAD+. Hypohydroxymethylation was observed in mtDNA. The 5-mC of mtDNA, 5mC of nDNA and nuclear and mtDNA adducts did not show differences after PCBs exposure. For the testicles, significant reductions in the levels of glutamate, malate, succinate, fumarate and NADH/NAD+ ratio were observed. The PCBs also induced hypohydroxymethylation in mtDNA and hypermethylation in nDNA, but there were no changes of 5-mC in mtDNA and 5-hmC in nDNA. A reduction of nDNA adducts 8-oxodG was observed. No changes were observed in the level of MDA and DNA adducts of nDNA. However, after PCBs exposure there was a significant decrease of 5-mC in global DNA of spermatozoa. The lower bound confidence interval on BMD, which were estimated for these markers can be used in the risk assessment of PCBs. Collectively, the data obtained in this study indicate that Aroclor 1254 induces alteration of intermediate metabolites, epigenetic marks and oxidative stress. These changes can adversely affect cells and cellular pathways, therefore increase the risk of cell death or transformation.

As bifenilas policloradas (PCBs) são um grupo de compostos hidrocarbonetos halogenados aromáticos, bioacumulativos em organismos vivos e persistente no ambiente. Além da atividade disruptora endócrina, os PCBs podem aumentar os níveis de espécies reativas de oxigênio (ROS), levando ao estresse oxidativo e alteração da metilação de DNA que são fatores importantes nas etiologias da hepatotoxicidade, infertilidade masculina e doença renal. Estes agentes tóxicos podem causar disfunção mitocondrial e distúrbios que afetam a produção de ATP, ROS e morte celular, ocasionando danos à saúde humana. O presente trabalho tem como objetivo investigar possíveis alterações genotóxicas e epigenéticas causadas pelo aroclor 1254 em fígado, rim e testículo, além de verificar a indução de estresse oxidativo e disrupção dos metabólitos intermediários do ciclo de Krebs nos referidos tecidos. Camundongos machos C57/BL6 foram expostos ao Aroclor 1254 em diferentes doses (5, 50, 500 e 1000 ug/kg) por gavagem, uma vez a cada três dias, durante 50 dias. Após a exposição, os animais foram eutanasiados, os órgãos coletados e espermatozoides obtidos a partir dos epidídimos. A peroxidação lipídica em plasma e tecidos foi avaliada pela quantificação de malonaldeído (MDA) por HPLC/DAD. Os níveis de intermediários da via glicolítica, do ciclo de Krebs, de alguns nucleotídeos e aminoácidos, marcas epigenéticas (5-mC e 5-hmC) e adutos de DNA (8-oxodG e CEdG) foram quantificados por HPLC-ESI-MS/MS. A abordagem de benchmark dose (BMD) foi utilizada para a modelagem dose resposta. Após exposição, não foram observadas diferenças significativas da variação da massa corporal, e a razão do peso testicular, fígado e rim por massa corporal. No tecido hepático, foi observado aumento da peroxidação lipídica. Houve redução significativa dos níveis de ATP, ADP, razão NADP+/NADPH, piruvato, malato, fumarato e glutamato. Observou-se redução significativa dos níveis de 5-mC e 5-hmC no DNA nuclear (nDNA), enquanto não foram observadas alterações dos níveis dos adutos. Em DNA mitocondrial (mtDNA) não foram observadas alterações nas marcas epigenéticas, no entanto foi obtido aumento significativo no aduto 8-oxodG após exposição ao Aroclor 1254. No tecido renal foi observado aumento significativo de MDA. Houve aumento significativo dos níveis de lactato e malato e reduções de ATP, ADP, glutamina, NAD+. Foi observada a hipohidroximetilação do mtDNA. As marcas 5-mC de mtDNA, 5mC de nDNA e adutos de DNA nuclear e mitocondrial não apresentaram diferenças após exposição a PCBs. Nos testículos foi verificada redução significativa dos níveis de glutamato, malato, succinato, fumarato e razão NADH/NAD+, hipohidroximetilção em mtDNA e hipermetilação em nDNA. Não foram observadas alterações de 5-mC em mtDNA e 5hmC em nDNA. Não foram verificadas alterações dos níveis de MDA e adutos em nDNA. Adicionando, foi observada redução dos níveis de 5-mC em DNA global de espermatozoide. Os limites inferiores do intervalo de confiança da BMD foram estimados para que estes marcadores possam ser usados na avaliação de riscos de PCBs. Os dados obtidos apontam o Aroclor 1254 como indutor de alterações do metabolismo intermediário, das marcas epigenéticas e estresse oxidativo. Essas alterações podem afetar vias celulares, levando à morte ou transformação, e aumentando o risco de doenças. / Polychlorinated biphenyls (PCBs) are a group of aromatic halogenated hydrocarbon compounds, which bioaccumulate in living organisms and is persistent in the environment. Besides their endocrine disrupting activity, PCBs may increase the levels of reactive oxygen species (ROS), leading to oxidative stress and alter DNA methylation that are important factors in the etiology of liver toxicity, male infertility, and kidney disease. These toxic agents can cause mitochondrial dysfunction and disorders that affect the production of ATP, ROS and cell death, thereby leading to health-related problems. The present work aimed at investigating possible genotoxic and epigenetic changes caused by aroclor 1254 in the liver, kidney and testis, as well as determine the induction of oxidative stress and disruption of intermediate metabolites in these tissues. Male C57/BL6 mice were exposed to Aroclor 1254 at different doses (5, 50, 500 and 1000 µg/kg) by gavage, once every three days, for 50 days. After the exposure period, the animals were euthanized, organs collected, and sperms obtained from the epididymis. Lipid peroxidation in plasma and tissues was determined by quantification of malonaldehyde (MDA) using HPLC/DAD. The levels of intermediate metabolites, epigenetic marks (5-mC and 5-hmC) and DNA adducts (8-oxodG and CEdG) were quantified by HPLC-ESI-MS/MS. The Benchmark dose approach (BMD) was used for dose response modeling. No significant differences in body weight variation, testicular, liver and kidney weight to body weight ratio were observed after exposure. However, in hepatic tissues, an increase in lipid peroxidation was observed. There were significant decreases in the intermediate metabolites including the levels of ATP, ADP, pyruvate, NADP+/NADPH ratio, malate and fumarate, as well as glutamate. Significant reduction of 5-mC and 5-hmC levels in nuclear DNA (nDNA) were observed, whereas no changes were observed in DNA adducts. The epigenetic marks in mitochondrial DNA (mtDNA) were not changed; however, a significant increase was observed in 8-oxodG adduct after exposure to Aroclor 1254. In renal tissues, data showed a significant increase in MDA, while for the intermediate metabolites, the levels of lactate and malate were significantly elevated, whereas significant reductions were recorded for ATP, ADP, glutamine, and NAD+. Hypohydroxymethylation was observed in mtDNA. The 5-mC of mtDNA, 5mC of nDNA and nuclear and mtDNA adducts did not show differences after PCBs exposure. For the testicles, significant reductions in the levels of glutamate, malate, succinate, fumarate and NADH/NAD+ ratio were observed. The PCBs also induced hypohydroxymethylation in mtDNA and hypermethylation in nDNA, but there were no changes of 5-mC in mtDNA and 5-hmC in nDNA. A reduction of nDNA adducts 8-oxodG was observed. No changes were observed in the level of MDA and DNA adducts of nDNA. However, after PCBs exposure there was a significant decrease of 5-mC in global DNA of spermatozoa. The lower bound confidence interval on BMD, which were estimated for these markers can be used in the risk assessment of PCBs. Collectively, the data obtained in this study indicate that Aroclor 1254 induces alteration of intermediate metabolites, epigenetic marks and oxidative stress. These changes can adversely affect cells and cellular pathways, therefore increase the risk of cell death or transformation.

Polychlorinated biphenyls (PCBs) are toxic and persistent anthropogenic contaminants. Concern on their adverse health effects has led to their regulation in air, water and/or soil in addition to sludge. Hence, removal of PCBs in various matrices, including transformer oils (TO) is a priority. This study aims to investigate PCB-118 and Aroclor 1254 toxicity and dechlorination by varying certain critical experimental components including electron donor (sludge or fatty acids), inocula (unacclimated or acclimated culture) and the doses of PCB and TO under anaerobic conditions. Anaerobic toxicity assays (ATA) reactors, lab-scale anaerobic batch digesters and sediment microcosms were used for this purpose. Increase in PCB-118 and TO doses affected anaerobic digester performance by negatively influencing methanogenesis, while favoring dechlorination only with the increase in PCB-118 dose. Up to 22% PCB-118 removal was attained with unacclimated culture. Studies with acclimated cultures showed Grasse River (GR) sediment to be the most active when compared to Fox River and Baltimore Harbor sediments. In GR sediment microcosms, PCB-118 and Aroclor 1254 removal efficiencies decreased when TO was present (1%), while 10% TO inhibited PCB dechlorination. Waste activated sludge was shown to be an effective electron donor, similar to fatty acids. Aroclor 1254 dechlorination was dechlorinated through removal of flanked meta and para chlorines, however, dechlorination pathways appeared to differ according to the presence/absence of TO. No ortho or unflanked chlorines were removed. Molecular tools (qPCR and DHPLC) were used to confirm the presence of active PCB dechlorinators. Dechlorination of PCBs was shown to be growth-linked.

This dissertation examines the patronage of Marie de Brabant, queen of France (1260-1322), and how her commissions transformed the atmosphere of the late Capetian court. Bringing with her from her native duchy of Brabant an established set of cultural preferences strikingly different from those that the saintly Louis IX had promoted in Paris for the previous half century, she introduced a love of secular material and elaborate ceremony upon her arrival in 1274. Taking the form of manuscript illumination, sculpture, stained glass, and architecture, as well as literature, music, science, history, genealogy, ritual, and finery, Marie’s patronage set a trend for courtly consumption for the remainder of the medieval period. Nearly always political in nature, her commissions were nonetheless sumptuous to behold, whether secular or sacred in content and they announced her status as Carolingian princess and French queen. Analysis of the frontispiece of Bibliothèque de l’Arsenal Ms. 3142, a richly illuminated miscellany of fictional, historical, and didactic poetry is crucial for understanding Marie’s taste and priorities, and is complemented by study of her other commissions in Brabant and France. These commissions varied from large scale -- such as the addition of chapels to the east end of the church of Notre-Dame in Mantes or window programs for the chapel of St. Nicholas at the church of St.-Nicaise in Reims and her parent’s necropolis at the church of the Dominicans in Louvain -- to smaller format -- the châsse of Ste. Gertrude at Nivelles or the donor statues of the chapelle de Navarre at Mantes. Most numerous, however, are the manuscripts that made up her diverse library which included the secular romances of Adenet le Roi and the scientific treatises of Guillaume de Nangis as well as historical and religious texts all of which were illuminated by the most renowned and creative artists of the day. After an analysis of her patronage as queen and widow, I look to how her activities as patron and collector influenced other late Capetian royal women, many of whom Marie had raised and whose activities, in turn, complemented and complicated their mentor’s vision of queenship. / text

Not available / text

PCBs are synthetic organic compounds known for their toxicity to many organisms and are notorious for having large discrepancies between measured and nominal concentrations. Historically thought to be less toxic, non-dioxin-like (NDL) PCBs represent the majority of congeners and are capable of eliciting neurotoxic effects. NDL-PCBs remain understudied, including their effects on aquatic organisms. In the first study, I collected extensive chemistry data and data on neurobehavioral and cardiac endpoints to test the acute effects of exposure to an NDL-PCB mixture on early life stage zebrafish. Neurobehavioral effects observed in the first study indicated a potential for longer term behavioral effects in these fish. In the second study, I collected data on feeding, social, and memory behavior of zebrafish at time points beyond the acute exposure from the first study. Acute and longer-term behavioral endpoints in the first and second studies demonstrated effects from PCB exposure but did not indicate mechanisms. In the third study, I collected untargeted and targeted metabolomic data on amino acid, sugar, anionic compound, and neurotransmitter profiles to determine the specific pathways affected by exposure to an NDL-PCB mixture. These combined data from these studies provide a unique insight into the chemical profile of an NDL-PCB mixture in biological applications and synthesize acute, longer-term, and mechanistic effects on developing zebrafish. These data fully illustrate an adverse outcome pathway from toxicokinetic to population level effects.

No description available.