Johannes Brahms is an important composer of 19th Century German. His music style inherits from the classical form, symmetric equilibrium, and blend with the romantic spirit. His unique music language includes, ¡§variable rhythm¡¨, ¡§transform, and combination of motive¡¨, ¡§extension, and transition of phrases¡¨, as well as the ¡§application of modulations, and cadences¡¨. These unique characteristics make his music colorful. Although Brahms¡¦ music does not have the brilliant techniques, and dramatic contrasts, but his work still finds its own position in the romantic period. In the later period of Brahms, his work breaks free from the prolonged, massive, and complicated scale, and transforms into the simple form with no technique emphasized piano pieces. During this period, Brahms¡¦ music is written by his free and unrestrained ideas. Sometimes, he would combine some literature in order to reinforce the depth of music conception. Klavierstücke op. 118 is composed in 1893, it is published at the same time with op. 119. They are both the last piano pieces. In op. 118, lots of moods change in these 6 pieces, for example, passion, enthusiasm, tenderness, excitement, grace, sadness¡Ketc, as if you are experiencing one person¡¦s life. Brahms connects different kinds of emotions together to allow audience experience all these feelings within one time. The first chapter of this thesis is to briefly go through the influence, and importance of Brahms in the music history, and to introduce the important piano pieces in each period. The second chapter is to analyze the music structure, theme, motive, harmony, and modulations of Klavierstücke op. 118. The focus of third chapter is on the performance practice of expression marks, characteristics of each voice, and the application of pedal.

Th. 3e cycle--Instrumentation nucl.--Grenoble 1, 1978. N°: 144.

No description available.

Thesis advisor: Brian P. Dunkle / The reception of the Mosaic Law was a source of perplexity for ancient Christians. The New Testament cites several of the laws set forth in the Books of Exodus, Leviticus, Numbers, and Deuteronomy (Mt 5:27, Lk 10:25-27, and 1 Cor 9:9-10). Yet the New Testament also suggests that the Mosaic legislation has been mitigated or abrogated (Acts 10, Rom 7:14, and Heb 10:1). Justin Martyr and Irenaeus of Lyon recount second century debates with Marcionites and Valentinians concerning the status of the Mosaic Law in ancient Christianity. This dissertation analyzes how similar debates played out in third and fourth-century interpretations of Psalm 118, an alphabetical acrostic whose 176 verses praise God’s laws (νόμος), commandments (ἐντολή), ordinances (δικαίωμα), testimonies (μαρτύριον), and judgments (κρίμα). Judith Lieu’s question – “Whose Marcion?” – provides a critical point of departure for this study, which focuses on how patristic authors conceptualized and attacked their own conceptions of “Marcion,” rather than on Marcion as an historical figure. Thus, Origen’s extant fragments from his commentary on Psalm 118, the earliest that survives, should be read within the context of his anti-Marcionite, Caesarean, exegetical homilies on the Books of Exodus, Leviticus, and Numbers. Using hermeneutical methods that systematize his attacks on Marcion, Origen inaugurated the anti- Marcionite tradition of interpretating Psalm 118 by emphasizing the figurative interpretation of the Mosaic Law, God’s role in teaching it, and the possibility of spiritual progress through understanding and acting on it. Origen, drawing on Philo of Alexandria’s figurative interpretations of the Pentateuch, responds to the Marcionite challenge by describing the contemplation of the Mosaic Law as a foundation for Christian ethics. During the fourth century, two western bishops – Hilary of Poitiers and Ambrose of Milan – received and developed Origen’s anti-Marcionite interpretation of Psalm 118. This study argues that both Hilary and Ambrose retain the anti-Marcionite orientation of Origen’s commentary and respond to the emergent threat posed by the Manichaeans, who in turn received and developed the Marcionites’ antinomian challenge. Hilary builds on Origen’s exegesis of Psalm 118 by describing divine law as a remedy for infirmitas. Hilary’s Tractatus on Psalm 118 recapitulates the main themes of Origen’s interpretation while giving greater emphasis to themes of theological anthropology. Rather than contemplation, Hilary calls for “exercise” (μελέτη/exercitiō) in the law as a means of Christian formation. Unlike his predecessors, Ambrose explicitly attacks Marcion in his Expositio on Psalm 118, unveiling the anti-heretical bearings of the tradition inaugurated by Origen. Ambrose comments on Psalm 118 within the liturgical context of offering post-baptismal catechesis to neophytes. Ambrose builds on Origen’s exegesis of Psalm 118 by describing David – the author of the Psalter – as an exemplary exegete of the figurative sense of the Mosaic Law. For the benefit of the neophytes, Ambrose contrasts David’s understanding of the Mosaic Law with the misunderstandings of the Marcionites, Manichaeans, and Jews. This study shows that the anti-Marcionite tradition of commenting on Psalm 118 was ultimately overshadowed in the fifth century and afterwards by Augustine’s anti-Pelagian Enarratio in Psalmum 118. Yet the anti- Marcionite tradition – which teaches Christians to read and profit spiritually from the Mosaic Law – is worthy of recovery. / Thesis (PhD) — Boston College, 2024. / Submitted to: Boston College. Graduate School of Arts and Sciences. / Discipline: Theology.

The thesis Psalm 118: Exegesis and Interpretation deals with the exegesis of a biblical text Psalm 118 (LXX 117). It approaches the psalm from various perspectives (both synchronic and diachronic) and giving compact exegesis. Thus the first focus of the thesis is the text itself, its different variants and its conceivable translation. Then, there is the stylistic-poetic analysis showing stylistic and poetic elements and also the connections between expressions of the psalm. Thus it is possible to understand the logic flow of the text, its structure. Then the thesis determines the genre of the psalm in order to make clear in what way and form the psalm expresses itself. Thanks to that it is possible to do more elaborate exegesis of several motives and poetic images that can be found in the text. Another perspective of the exegesis of the psalm is to consider its musical denotation. Next part is concerned by how the text fits within the context of the Psalter and the Hebrew bible and also the outline of its basic ways in its history of influence.

ITC/USA 2007 Conference Proceedings / The Forty-Third Annual International Telemetering Conference and Technical Exhibition / October 22-25, 2007 / Riviera Hotel & Convention Center, Las Vegas, Nevada / The most recent version of IRIG 118, Test Methods for Telemetry Systems and Subsystems, was released in 1999 and does not include any guidance for testing IRIG 106 Chapter 10 recorder / reproducers. This paper will describe the methodology and tools used to perform a thorough testing process to ensure compliance with the IRIG 106-07 standard.

<p>The Ras family of small GTPases, comprised of the KRAS, NRAS, and HRAS genes, are mutated to encode constitutively-active, GTP-bound, oncogenic proteins in upwards of one quarter or more of all human cancers, which is well established to promote tumorigenesis. Despite the prominent role these genes play in human cancer, the encoded proteins have proven difficult to pharmacologically inhibit. Therefore, it is important to understand how Ras proteins are activated. </p><p>RAS proteins cycle between a GDP-bound inactive state and a GTP-bound active state through guanine nucleotide exchange factors (GEFs) and GTPase activating proteins (GAPs). GEFs facilitate the GDP-to-GTP exchange of RAS and promote RAS activation. Similar to GEFs, reactive oxygen/nitrogen species can also promote RAS activation through reactions with the thiol residue of cysteine 118 (C118). This residue may therefore play a role in RAS activation in cancer. To test this possibility, I investigated the effect of mutating C118 to serine (C118S) in Kras on (1) carcinogen-induced lung tumorigenesis, and (2) xenograft tumor growth of HRAS12V-transformed cells.</p><p>To explore the impact of the C118S mutation in Kras on carcinogen-induced lung tumorigenesis, I introduced a C118S mutation into the endogenous murine Kras allele and exposed the resultant mice to the carcinogen urethane, which induces Kras mutation-positive lung tumors. Kras+/C118S and KrasC118S/C118S mice developed fewer and smaller lung tumors than Kras+/+ mice. Although the KrasC118S allele did not appear to affect tumorigenesis when the remaining Kras allele was conditionally oncogenic (KrasG12D), there was a moderate imbalance of oncogenic mutations favoring the native Kras allele in tumors from Kras+/C118S mice treated with urethane. Therefore, mutating C118 of Kras impedes urethane-induced lung tumorigenesis.</p><p>To explore the the impact of the C118S mutation in Kras on xenograft tumor growth of HRAS12V-transformed cells, I tested and found that redox-dependent reactions with cysteine 118 (C118) and activation of wild type KRAS are critical for oncogenic HRAS-driven tumorigenesis. Such redox-dependent activation of KRAS affected both PI3K-AKT and RAF-MEK-ERK pathways. These findings were confirmed in the endogenous mouse Kras gene. Speicfically, oncogenic HRAS-transformed KrasC118S/C118S MEFs grew in soft agar and as xenograft tumors more slowly than similarly transformed Kras+/+ MEFs, suggesting that redox-dependent reactions with C118 of Kras promotes transformation and tumorigenesis. </p><p>Taken together, I have demonstrated a critical role of redox-dependent reactions with Kras C118 in tumorigenesis.</p> / Dissertation

Résumé / Abstract

Conselho Nacional de Desenvolvimento Científico e Tecnológico / Tem sido descrito que o acúmulo de mutações em proto-oncogenes e genes supressores de tumor contribui para o direcionamento da célula à carcinogênese. Na maioria dos casos de câncer, as células apresentam proliferação descontrolada devido a alterações na expressão e/ou mutações de ciclinas, quinases dependentes de ciclinas e/ou inibidores do ciclo celular. Os tumores sólidos figuram entre o tipo de câncer mais incidente no mundo, sendo a quimioterapia e/ou hormônio-terapia, radioterapia e cirurgia os tratamentos mais indicados para estes tipos de tumores. Entretanto, o tratamento quimioterápico apresenta diversos efeitos colaterais e muitas vezes é ineficaz. Portanto, a busca por novas moléculas capazes de conter a proliferação destas células e com baixa toxicidade para o organismo se faz necessário. Este trabalho teve por objetivo avaliar a ação antitumoral in vitro de um novo composto sintético, a pterocarpanoquinona LQB118, sobre algumas linhagens tumorais humanas de alta prevalência e estudar alguns dos seus mecanismos de ação. As linhagens tumorais estudadas neste trabalho foram os adenocarcinomas de mama (MCF7) e próstata (PC-3), e carcinoma de pulmão (A549). A citotoxicidade foi avaliada pelo ensaio do MTT e a proliferação celular pela contagem de células vivas (exclusão do corante azul de tripan) e análise do ciclo celular (citometria de fluxo). A expressão gênica foi avaliada por RT-PCR e a apoptose foi avaliada por condensação da cromatina (microscopia de fluorescência-DAPI), fragmentação de DNA (eletroforese) e marcação com anexina V (citometria de fluxo). Das linhagens tumorais testadas, a de próstata (PC3) foi a que se mostrou mais sensível ao LQB 118, e em função deste resultado, os demais experimentos foram realizados com esta linhagem tumoral. O efeito citotóxico do LQB 118 se mostrou tempo e concentração dependente. Esta substância inibiu a proliferação celular e prejudicou a progressão do ciclo celular, acumulando células nas fases S e G2/M. Buscando esclarecer os mecanismos desta ação antitumoral, demonstrou-se que o LQB 118 inibe a expressão do mRNA do fator de transcrição c-Myc e das ciclinas D1 e B1, e induz a apoptose de tais células tumorais. Em suma, o LQB 118 é capaz de inibir a proliferação das células tumorais de próstata, alterando a expressão do mRNA de alguns genes reguladores do ciclo celular, resultando em interrupção do ciclo celular e indução de apoptose, indicando este composto como um potencial candidato a futuro medicamento no tratamento do câncer de próstata. / It has been reported that accumulation of mutation on proto-oncogenes and tumor suppressor genes directs cells to carcinogenesis. In most described cancer, cells display uncontrolled proliferation due to altered expression or mutations of cyclins, cyclin-dependent kinases and cell cycle inhibitors. The solid tumors are the most common cancer type in world. Chemotherapy and/or hormone-therapy, radiotherapy and surgery are the suitable treatment for this disease. However, chemotherapy has been shown several side effects and often ineffective. Therefore, the search for new molecules with antitumoral activity low cytotoxicity is needed. The aim of this work was to evaluate the in vitro antitumoral effects of a new synthetic compound, the pterocarpanquinone LQB 118, on tumor cell lines of high prevalence in the world and to study some mechanisms of action. Tumor cell lines of breast (MCF7), lung (A549) and prostate (PC3) were cultivated at RPMI medium with 10% of serum fetal bovine. The cytotoxicity was evaluated by MTT assay and the cell proliferation by cell counting (trypan blue exclusion) and cell cycle analysis (flow cytometry). Apoptosis was evaluated by chromatin condensation (fluorescence microscopy with DAPI), DNA fragmentation (electrophoresis) and annexin-V and iodide propidium staining. Gene expression was studied by RT-PCR. As LQB 118 (5 g/ml) induced cytotoxic effect mainly on prostate tumor cells, further experiments were then performed only with this tumor cell line. The LQB 118 cytotoxic effects were time and concentration-dependent. Furthermore, this substance inhibited cell proliferation and promoted cell cycle arrest, increasing cell number in S and G2/M phases. Studying the mechanisms of the LQB 118 antitumoral action, it was demonstrated that this substance inhibited the mRNA expression of the transcription factor c-Myc, cyclin D1 and cyclin B1 and also induced apoptosis of PC3. Concluding, LQB 118 impairs prostate tumor cells proliferation due to altered mRNA expression of some cell cycle regulator genes, resulting in cell cycle arrest and apoptosis induction, suggesting this compound as a good candidate for a future drug in prostate cancer treatment.

Conselho Nacional de Desenvolvimento Científico e Tecnológico / Tem sido descrito que o acúmulo de mutações em proto-oncogenes e genes supressores de tumor contribui para o direcionamento da célula à carcinogênese. Na maioria dos casos de câncer, as células apresentam proliferação descontrolada devido a alterações na expressão e/ou mutações de ciclinas, quinases dependentes de ciclinas e/ou inibidores do ciclo celular. Os tumores sólidos figuram entre o tipo de câncer mais incidente no mundo, sendo a quimioterapia e/ou hormônio-terapia, radioterapia e cirurgia os tratamentos mais indicados para estes tipos de tumores. Entretanto, o tratamento quimioterápico apresenta diversos efeitos colaterais e muitas vezes é ineficaz. Portanto, a busca por novas moléculas capazes de conter a proliferação destas células e com baixa toxicidade para o organismo se faz necessário. Este trabalho teve por objetivo avaliar a ação antitumoral in vitro de um novo composto sintético, a pterocarpanoquinona LQB118, sobre algumas linhagens tumorais humanas de alta prevalência e estudar alguns dos seus mecanismos de ação. As linhagens tumorais estudadas neste trabalho foram os adenocarcinomas de mama (MCF7) e próstata (PC-3), e carcinoma de pulmão (A549). A citotoxicidade foi avaliada pelo ensaio do MTT e a proliferação celular pela contagem de células vivas (exclusão do corante azul de tripan) e análise do ciclo celular (citometria de fluxo). A expressão gênica foi avaliada por RT-PCR e a apoptose foi avaliada por condensação da cromatina (microscopia de fluorescência-DAPI), fragmentação de DNA (eletroforese) e marcação com anexina V (citometria de fluxo). Das linhagens tumorais testadas, a de próstata (PC3) foi a que se mostrou mais sensível ao LQB 118, e em função deste resultado, os demais experimentos foram realizados com esta linhagem tumoral. O efeito citotóxico do LQB 118 se mostrou tempo e concentração dependente. Esta substância inibiu a proliferação celular e prejudicou a progressão do ciclo celular, acumulando células nas fases S e G2/M. Buscando esclarecer os mecanismos desta ação antitumoral, demonstrou-se que o LQB 118 inibe a expressão do mRNA do fator de transcrição c-Myc e das ciclinas D1 e B1, e induz a apoptose de tais células tumorais. Em suma, o LQB 118 é capaz de inibir a proliferação das células tumorais de próstata, alterando a expressão do mRNA de alguns genes reguladores do ciclo celular, resultando em interrupção do ciclo celular e indução de apoptose, indicando este composto como um potencial candidato a futuro medicamento no tratamento do câncer de próstata. / It has been reported that accumulation of mutation on proto-oncogenes and tumor suppressor genes directs cells to carcinogenesis. In most described cancer, cells display uncontrolled proliferation due to altered expression or mutations of cyclins, cyclin-dependent kinases and cell cycle inhibitors. The solid tumors are the most common cancer type in world. Chemotherapy and/or hormone-therapy, radiotherapy and surgery are the suitable treatment for this disease. However, chemotherapy has been shown several side effects and often ineffective. Therefore, the search for new molecules with antitumoral activity low cytotoxicity is needed. The aim of this work was to evaluate the in vitro antitumoral effects of a new synthetic compound, the pterocarpanquinone LQB 118, on tumor cell lines of high prevalence in the world and to study some mechanisms of action. Tumor cell lines of breast (MCF7), lung (A549) and prostate (PC3) were cultivated at RPMI medium with 10% of serum fetal bovine. The cytotoxicity was evaluated by MTT assay and the cell proliferation by cell counting (trypan blue exclusion) and cell cycle analysis (flow cytometry). Apoptosis was evaluated by chromatin condensation (fluorescence microscopy with DAPI), DNA fragmentation (electrophoresis) and annexin-V and iodide propidium staining. Gene expression was studied by RT-PCR. As LQB 118 (5 g/ml) induced cytotoxic effect mainly on prostate tumor cells, further experiments were then performed only with this tumor cell line. The LQB 118 cytotoxic effects were time and concentration-dependent. Furthermore, this substance inhibited cell proliferation and promoted cell cycle arrest, increasing cell number in S and G2/M phases. Studying the mechanisms of the LQB 118 antitumoral action, it was demonstrated that this substance inhibited the mRNA expression of the transcription factor c-Myc, cyclin D1 and cyclin B1 and also induced apoptosis of PC3. Concluding, LQB 118 impairs prostate tumor cells proliferation due to altered mRNA expression of some cell cycle regulator genes, resulting in cell cycle arrest and apoptosis induction, suggesting this compound as a good candidate for a future drug in prostate cancer treatment.