1,248 research outputs found
Brenner 2020 – Ntano – Audio 3
No full textMontage by Klaus-Peter Brenner of two audio tracks: (1) Malaŵian Sena ntano polyphonic multi-part singing. Track B3 from Gerhard Kubik and Moya Aliya Malamusi (1989), Südliches Malaŵi. Musiker aus Malaŵi. “Opeka nyimbo” Musiker-Komponisten. / Southern Malaŵi: Musicians from Malaŵi. “Opeka nyimbo” Musician-composers. Berlin: Musikethnologische Abteilung, Museum für Völkerkunde Berlin, Staatliche Museen Preußischer Kulturbesitz. MC 15. Double LP. (2) Excerpt of the Shona mbira dzavadzimu piece “Nhemamusasa”, kushaura and kutsinhira parts both played by the author; one harmonic cycle extracted, looped and tempo digitally increased according to the original tempo of recording (1). Excerpts of both tracks are looped and digitally superimposed in order to demonstrate their remarkable degree of structural congruence. Discussion of the montage in Klaus-Peter Brenner (2020), “A Grammatical Merger of Heterogeneous Musical Structures: The Vocal Polyphony Ntano of the Sena of Southern Malaŵi.” In Understanding Musics: Festschrift on the Occasion of Gerd Grupe\u27s 65th Birthday, ed. Malik Sharif and Kendra Stepputat, 125–151. Düren: Shaker
Cosmoscepsia Catholica, Das ist/ Allgemeiner Weltlauff/ und was sich denckwürdiges unnd newes in der gehelen gantzen Welt/ sowol in Geistlichen als Weltlichen Sachen verlauffen und zugetragen / Mit schönen Kupfferstücken gezieret/ und in Truck gegeben: Durch M. Sebastianum Prennern ...
No full textWendy Brenner
No full textWendy Brenner visited The College at Brockport in October 1996. She is an author and professor of Creative Writing.Archived web contentSUNY BrockportWriters Forum Author Photo
Wendy Brenner
No full textWendy Brenner visited The College at Brockport in October 1996. She is an author and professor of Creative Writing.https://digitalcommons.brockport.edu/writers_photos/1007/thumbnail.jp
Therapeutic Targeting the Cell Division Cycle 25 (CDC25) Phosphatases in Human Acute Myeloid Leukemia — The Possibility to Target Several Kinases through Inhibition of the Various CDC25 Isoforms
No full textThe cell division cycle 25 (CDC25) phosphatases include CDC25A, CDC25B and CDC25C. These three molecules are important regulators of several steps in the cell cycle, including the activation of various cyclin-dependent kinases (CDKs). CDC25s seem to have a role in the development of several human malignancies, including acute myeloid leukemia (AML); and CDC25 inhibition is therefore considered as a possible anticancer strategy. Firstly, upregulation of CDC25A can enhance cell proliferation and the expression seems to be controlled through PI3K-Akt-mTOR signaling, a pathway possibly mediating chemoresistance in human AML. Loss of CDC25A is also important for the cell cycle arrest caused by differentiation induction of malignant hematopoietic cells. Secondly, high CDC25B expression is associated with resistance against the antiproliferative effect of PI3K-Akt-mTOR inhibitors in primary human AML cells, and inhibition of this isoform seems to reduce AML cell line proliferation through effects on NFκB and p300. Finally, CDC25C seems important for the phenotype of AML cells at least for a subset of patients. Many of the identified CDC25 inhibitors show cross-reactivity among the three CDC25 isoforms. Thus, by using such cross-reactive inhibitors it may become possible to inhibit several molecular events in the regulation of cell cycle progression and even cytoplasmic signaling, including activation of several CDKs, through the use of a single drug. Such combined strategies will probably be an advantage in human cancer treatment
CDC25 Inhibition in Acute Myeloid Leukemia-A Study of Patient Heterogeneity and the Effects of Different Inhibitors
No full textCell division cycle 25 (CDC25) protein phosphatases regulate cell cycle progression through the activation of cyclin-dependent kinases (CDKs), but they are also involved in chromatin modulation and transcriptional regulation. CDC25 inhibition is regarded as a possible therapeutic strategy for the treatment of human malignancies, including acute myeloid leukemia (AML). We investigated the in vitro effects of CDC25 inhibitors on primary human AML cells derived from 79 unselected patients in suspension cultures. Both the previously well-characterized CDC25 inhibitor NSC95397, as well as five other inhibitors (BN82002 and the novel small molecular compounds ALX1, ALX2, ALX3, and ALX4), only exhibited antiproliferative effects for a subset of patients when tested alone. These antiproliferative effects showed associations with differences in genetic abnormalities and/or AML cell differentiation. However, the responders to CDC25 inhibition could be identified by analysis of global gene expression profiles. The differentially expressed genes were associated with the cytoskeleton, microtubules, and cell signaling. The constitutive release of 28 soluble mediators showed a wide variation among patients and this variation was maintained in the presence of CDC25 inhibition. Finally, NSC95397 had no or only minimal effects on AML cell viability. In conclusion, CDC25 inhibition has antiproliferative effects on primary human AML cells for a subset of patients, and these patients can be identified by gene expression profiling
Mitteilungen aus dem Brenner-Archiv / Stirne an Stirne : Zu zwei Briefen Christine Lavants an Hermann Lienhard
No full textMitteilungen aus dem Brenner-Archiv / Stirne an Stirne : Zu zwei Briefen Christine Lavants an Hermann Lienhard
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