24,539 research outputs found
Jack Alive / Martin Dead : The Location of the "Author" in Jack London\u27s Martin Eden
No full textThis essay is an attempt to read Martin Eden, Jack Londonʼs autobiographical novel, in terms of the inextricable relationship between the author and the protagonist. Critics have often taken the unbalanced plot and the lack of ironic distance between narrator and character in Martin Eden as the technical weakness of London, but this paper argues that the achievement of this novel owes a great deal to the attachment of London to Martin. The unbalanced structure is a necessary product of the severe struggle of the author to kill his romantic alter ego. // Martin, who aspires to win Ruth Morse, tries to cross class boundaries by making a career of a writer. Even after realizing the emptiness of Ruth, who turns out to be nothing but a typical figure of the bourgeoisie, he somehow persists in loving her. The notion underlying here is that, for Martin, love, career and art are fundamentally inseparable. He objects to the aestheteʼs view of Brissenden on account of his separation of art from career. Martinʼs identity and life consist only in the triunity of love/career/art; the alternative is the repudiation of life. Thus, the unnatural delay of his disappointment in love can be regarded as Londonʼs strategy to set the suicide of Martin as the necessary consequence of the story. // By finishing the story and killing Martin, London finally detaches himself from Martin, reconstructs his self, and, unlike Martin, survives as a professional writer. In this sense, Martin Eden is a story about “writerʼs self-reconstruction.
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Letter from Martin Chizzick
No full textCongratulations to Duane Pearsall for receiving the Enterpreneur of the Year award; note on the letter was written by Pearsall and it mentions that Martin, the author of the letter, died in a airplane accident
Robert Martin Tiffin's Mystery Man Newspaper Articles
No full textAdvertiser-Tribune newspaper clippings featuring a story about Robert Martin (written by Nancy Kleinhenz), a local author from Tiffin (Ohio) who wrote under the pseudonym of Lee Roberts, and two of his short stories. Martin wrote mystery novels in his spare time, creating more than 22 mystery novels. For more information about Robert Martin and a list of books go to http://www.mysteryfile.com/RMartin/JBennett.html
Experiences Using Large Scale Video Walls for Distance Education
No full textWe describe our experiences building and using the Rutgers Videowall, a low-cost telepresence system that has been used teaching 15 courses and colloquia. By relaxing typical spatial telepresence features, such as background continuity, we greatly reduced costs and gained flexibility in the rooms it could be deployed in. The lower costs and room flexibility enabled academic departments to use the wall, in contrast to traditional telepresence systems which remained inaccessible. We found that the Videowall’s spatial distortions did not have a significant impact on useability, as our initial survey results show that students had an overall positive experience.Technical report DCS-tr-72
Hans Martin Schwarz Collection 1934 - 1938
No full textThis collection contains clippings of articles by Hans Martin Schwarz (1917, Hamburg – 2006, New York, better known as Martin Ebon), published between 1934 and 1938 in German-Jewish newspapers on a wide variety of subjects such as sports, emigration, the political situation in Germany, and religious attitudes of the young. It also contains reviews of his books "Einer wie Du und Ich" and "Heiteres, Besinnliches, Nachdenkliches."digitizedHans Martin Schwarz (1917, Hamburg – 2006, New York, better known as Martin Ebon), was a journalist and author. In Germany during the 1930s, he published in a variety of German-Jewish periodicals, primarily the Israelitisches Familienblatt. After immigrating to the United States in 1938, he changed his name to Martin Ebon, and published dozens of books in the areas of world affairs and parapsychology.Processe
Interview with Father James Martin
No full textIn May 2011, the Ignatian Faculty Scholars at Regis University conducted a Skype interview with Father James Martin, S. J., author of The Jesuit Guide to Almost Everything. The Scholars had used Father Martin’s book as a text for their year of study, which focused on Ignatian Spirituality, the Ignatian Pedagogical Paradigm, and teaching and learning at a Jesuit university. The interview was transcribed and is printed below. Father Martin reflects on the book, and responds to questions about the book itself, about finding God in all learners, and about the Church
Short and long term radiation effects after ionizing radiation and its dependence on chromatin modification and repair inhibition in human lung cell lines
No full textThe dynamic nature of chromatin and its modifications play a critical role in transcriptional gene regulation and thus can affect several cellular functions such as differentiation, replication, DNA damage response and activation of cell death. Alterations in cellular epigenetic and genetic structure after IR can lead to long term effects, such as survival and genomic instability. Additionally, DSB repair is thought to be differentially regulated in euchromatin and heterochromatin. Histone methylation is an important modification related to the compactness and transcriptional activity of chromatin. Thus histone methyltransferases (HMT) play a pivotal role in determining the functional status of chromatin. The human HMT SUV39h1 and SUV39h2 are altered in various types of human cancers.
Here we show that the knockout Suv39h1/2 mice fibroblasts (Fbs) have significantly lower clonogenic survival, which is attributed to reduced DSB repair capacity of these cells. The downregulation of HMT SUV39H1 in human lung cancer cell lines leads to significantly reduced number of radiation-induced residual γH2AX. However, the effect of SUV39H1 downregulation on clonogenical survival was less marked as compared to the mouse knockout model. Additionally, the HMT inhibitor Chaetocin, significantly reduces the radiation dose necessary to control 50% of a plaque-monolayer culture after treatment with low concentrations, reduces the cell proliferation and significantly increased apoptosis in lung cancer cell lines. Moreover Chaetocin was found to remodel the nuclear chromatin structure by forming chaetocin-induced chromatin condensation/clustering which is mainly associated with heterochromatin domains in primary human Fbs, transformed mFbs and in the tumour cell line H1299
A synthetic lethality-based strategy for individual sensitization of lung cancer cell lines with vulnerability in the SWI/SNF complex to radiotherapy
No full textDie vorliegende Arbeit beschäftigt sich mit dem Einfluss der Chromatin-Remodellierung durch den SWI/SNF-Komplex auf die Strahlenantwort von Zellen. Dazu wurde die ATPase Untereinheit SMARCA2/BRM in SMARCA4/Brg1-mutierten und -wildtyp Zelllinien mittels siRNA depletiert und anschließend der Einfluss auf das Überleben der Zellen untersucht. In dieser Studie wird zum ersten Mal ein signifikanter Rückgang des klonogenen Überlebens nach BRM-Depletion in Kombination mit Bestrahlung von Brg1-mutierten NSCLC Zellen, im Gegensatz zu Brg1-profizienten NSCLC Zellen und Fibroblasten, gezeigt. In einem weiteren Überlebensassay, dem Minimonolayer assay, konnte eine Verschiebung der Dosis-Wirkungskurven nach einmaliger als auch nach fraktionierter Bestrahlung mit 4 Gy/Tag in den niedrigeren Dosisbereich nach BRM knock-down in Brg1-mutierten NSCLC Zelllinien nachgewiesen werden. Minimonolayer, die mittels fraktionierter Bestrahlung zweimal am Tag mit 4 Gy bestrahlt wurden, sodass die Repopulierung verringert wird und der Einfluss der Reparatur deutlich wird, zeigen nach BRM-Depletion eine anhaltende Verschiebung der Dosis-Wirkungskurve in den niedrigeren Dosisbereich. Interessanterweise zeigen die hier untersuchten Brg1-defizienten Zelllinien, im Vergleich zu den Brg1-profizienten, eine erniedrigte Strahlensensitivität. Ob die Expression des BRG1-Proteins als Biomarker für die Strahlensensitivität von NSCLC genutzt werden kann sollte daher in weiteren klinischen Studien näher untersucht werden.
Zusätzlich wurden die zugrundeliegenden Mechanismen der si-BRM induzierten Strahlensensitivierung Brg1-mutierter NSCLC Zelllinien evaluiert. Dazu wurde der Einfluss der BRM-Depletion auf die DNA-Doppelstrangbruch Reparatursignalwege NHEJ und HRR untersucht. Die Ergebnisse der γH2AX und 53BP1 Foci Analysen, die als Hinweis für NHEJ dienen, zeigen keinen signifikanten Unterschied in den Brg1-defizienten als auch in Brg1-profizienten NSCLC Zelllinien nach BRM knock-down. Die Untersuchung von HRR, die mittels Detektion von RAD51 Foci durchgeführt wurde, zeigte allerdings einen signifikanten Anstieg der residuellen RAD51 Foci in Brg1-defizienten NSCLC Zelllinien, sowohl über die gesamte Zellpopulation als auch in Cyclin B1-markierten Zellen.
Da die HRR nur in der S- und G2-Phase des Zellzyklusses stattfindet, wurde die Zelllinie A549 mit mutiertem Brg1 in unterschiedlichen Wachstumsphasen (G1-Phase bzw. S-Phase angereichert) bestrahlt und das klonogene Überleben nach BRM knock-down verglichen. Die Ergebnisse zeigen im Vergleich zur konfluenten Zellkultur eine erhöhte si-BRM induzierte Strahlensensitivität der exponentiell wachsenden Zellkultur. Die zusätzliche Anreicherung der Zellen in der S-Phase mittels Aphidicolin zeigt eine weitere Steigerung der Strahlenempfindlichkeit nach si-BRM in der Brg1-mutierten Zelllinie A549. Um auszuschließen, dass die NHEJ nicht am strahlensensitivierenden Effekt nach BRM-Depletion beteiligt ist, wurde das Schlüsselenzym der NHEJ, die DNA-PK inhibiert. Die Erhöhung der Strahlensensitivität nach BRM knock-down bleibt weiterhin bestehen. Anschließend wurde untersucht, ob die HRR an dem strahlensensitivierenden Effekt nach si-BRM beteiligt ist. Dazu wurde das Schlüsselenzym der HRR, RAD51, mittels siRNA depletiert. Die Ergebnisse zeigen keinen zusätzlichen si-BRM-Effekt in Kombination mit si-RAD51. Somit lässt sich schlussfolgern, dass die si-BRM induzierte strahlensensitivierende Wirkung von RAD51 abhängig ist. Aus den vorliegenden Ergebnissen lässt sich schlussfolgern, dass die Inhibition der ATPase Untereinheit SMARCA2/BRM einen neuen zielgerichteten Ansatz für die Therapie von SMARCA4/Brg1-mutierter Lungentumore darstellt.In this study we investigated the influence of the chromatin remodeling complex SWI/SNF on the radiation response of NSCLC cell lines. In this respect the expression of the ATPase subunit SMARCA2/BRM was depleted in SMARCA4/BRG1-mutated and wildtype cell lines by siRNA to evaluate the impact on the survival. This is the first study indicating increased radiation sensitivity specifically in BRG1-mutant but not BRG1-wild-type cell lines and fibroblasts after BRM depletion. The results of the mini monolayer assay, which is a tumor population survival assay, reveal that BRM depletion specifically increases the radioresponse of BRG1-deficient NSCLC cells after fractionated (4 Gy/day) as wells as single dose-irradiation in comparison to lipofectamine and non-target siRNA control. Mini monolayers of BRG1-mutant tumor cell lines irradiated two times per day with 4 Gy, thereby decreases the repopulation and increases the effect of DNA damage repair, show a persistent increase of radio response after BRM depletion. Interestingly, the results reveal that BRG1-mutated cell lines without expression of the full length BRG1 protein are significantly more resistant to ionizing radiation than cell lines without such mutation. Thus, if expression of BRG1 could be a potential biomarker for the radiation sensitivity of NSCLC should be further analyzed in clinical series.
To further analyze the underlying mechanism of the sensitizing effect after BRM depletion in BRG1-mutated NSCLC cell lines, influence on DNA double strand break repair pathways NHEJ and HRR was evaluated. The results of γH2AX and 53BP1 foci analysis, indicating DNA repair by NHEJ, show neither in BRG1-deficient nor in BRG1-proficient NSCLC cell lines significantly differences in foci formation after BRM depletion. However, a decreased resolution of Rad51 foci 24 h after BRM knockdown was found in BRG1-mutated cells regarding the whole cell population as well as Cyclin B1 (G2 phase cells) labeled cells. Because HRR is only restricted to S and G2 phase cells, the surviving fraction of BRM depleted A549 enriched G1 phase cells was compared to cells enriched in S phase after irradiation. The results indicate an increase in siBRM induced radio sensitivity in S phase enriched cell culture. BRG1-mutated A549 cells enriched in S phase with Aphidicolin reveal an additional enhancement of radiation sensitivity. Inhibition of DNA-PK, the key enzyme of NHEJ, leads to a persistent radiation sensitizing effect after BRM depletion that excludes an involvement of NHEJ in the siBRM induced radio sensitizing effect. To evaluate whether HRR, the other DSB repair pathway, is involved in radio sensitization after BRM depletion, the key enzyme RAD51 was depleted by siRNA. The results show no additional radio sensitization of siBRM in combination with siRAD51. In conclusion, the present study shows that SMARCA2/BRM depletion increases radiation responsiveness of SMARCA4/BRG1-mutated human NSCLC cell lines and thus identifies BRM as an interesting therapeutic target in SMARCA4/BRG1 mutant cancers
Benefits of a Classification Scheme of Granitic Pegmatites Based on Petrogenetic Considerations.
No full textOral presentation-
Communicating author: Martin RF
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