Motown Unreleased: 1969 [Various Artists]

Liner notes to support the digital release of the 2019 various artists collection Motown Unreleased: 1969https://digitalcommons.carleton.edu/motown_annotated_track_lists/1000/thumbnail.jp

The Ballads of Marvin Gaye

This article focuses on Marvin Gaye’s involvement with music related to the “middle of the road” (MOR) market within the American music business between 1961 and 1979. From 1961 to 1966, in addition to his work as a teen idol, Gaye performed regularly in supper clubs, released four albums of standards material, and recorded dozens of other related songs that were eventually shelved. In a fascinating turn, he worked extensively on a series of unreleased tracks between 1967 and 1979, using experimental techniques to revise, reinterpret, and recompose melodies over already completed backing music. Gaye’s interest in ballads connects to a different tradition of American music from his soul hits, drawing on the legacy of 1920s crooning, mainstream swing vocalists like Frank Sinatra, and African American forebears such as Nat “King” Cole and Sam Cooke. This article makes a number of new claims about Gaye’s career trajectory: that his method of composing with his voice in the studio—building up complex textures from multiple takes and composing lyrics and melody directly to tape—began as early as 1967, well before his better-known experiments for What’s Going On in 1970; that the popular, sexuality-charged music of his final decade was an extension of his work with romantic balladry in the 1960s; and that his interest in standards continued much farther into his career than is suggested by his official discography

A Tribute to the Great Nat King Cole [Expanded Edition]

Liner notes to support the digital release of the 1965 Marvin Gaye LP A Tribute to the Great Nat King Cole [Expanded Edition]https://digitalcommons.carleton.edu/marvin_gaye_annotated_track_lists/1000/thumbnail.jp

Concert recording 2015-04-04b

[Track 01]. Introduction and variations on a theme by Mozart, op. 9 / Fernando Sor -- [Track 02]. Xango / Luiz Bonfá -- [Track 03]. La cathedral. Preludio saudade ; [Track 04]. Andante religioso ; [Track 05]. Allegro solemne / Augustin Barrios -- [Track 06]. Prelude, Fugue ; [Track 07]. Allegro, BWV 998 / J.S. Bach -- [Track 08]. Koyunbaba. Movement I ; [Track 09]. Movement IV / Carlo Domeniconi

Spacetime as a quantum circuit

We propose that finite cutoff regions of holographic spacetimes represent quantum circuits that map between boundary states at different times and Wilsonian cutoffs, and that the complexity of those quantum circuits is given by the gravitational action. The optimal circuit minimizes the gravitational action. This is a generalization of both the "complexity equals volume" conjecture to unoptimized circuits, and path integral optimization to finite cutoffs. Using tools from holographic $T\bar T$, we find that surfaces of constant scalar curvature play a special role in optimizing quantum circuits. We also find an interesting connection of our proposal to kinematic space, and discuss possible circuit representations and gate counting interpretations of the gravitational action.Comment: 26 pages, 2 figure

Concert recording 2018-04-22d

[Track 1]. Trio for piano, oboe, and horn in A minor, op. 188. Allegro moderato [Track 2]. Scherzo [Track 3]. Adagio [Track 4]. Allegro ma non troppo / Carl Reinecke -- [Track 5]. Three nocturnes for cello and guitar / Frederic Burgmuller -- [Track 6]. Bagatelles for horn, bassoon and piano. March [Track 7]. Aria [Track 8]. Gamelan [Track 9]. Mirage [Track 10]. Polka / Paul Basler -- [Track 11]. Oblivion / Astor Piazzola arranged by Jeffrey Scott

Network development in biological gels: role in lymphatic vessel development

In this paper, we present a model that explains the prepatterning of lymphatic vessel morphology in collagen gels. This model is derived using the theory of two phase rubber material due to Flory and coworkers and it consists of two coupled fourth order partial differential equations describing the evolution of the collagen volume fraction, and the evolution of the proton concentration in a collagen implant; as described in experiments of Boardman and Swartz (Circ. Res. 92, 801–808, 2003). Using linear stability analysis, we find that above a critical level of proton concentration, spatial patterns form due to small perturbations in the initially uniform steady state. Using a long wavelength reduction, we can reduce the two coupled partial differential equations to one fourth order equation that is very similar to the Cahn–Hilliard equation; however, it has more complex nonlinearities and degeneracies. We present the results of numerical simulations and discuss the biological implications of our model

Concert recording 2013-12-04

[Track 01]. Omaggio / Manuel de Falla -- [Track 02]. Bossa cancao / Frank Basan -- [Track 03]. Spanish study / Frederick Noad -- [Track 04]. Adelita / Francisco Tarrega -- [Track 05]. Everything happens to me / Dennis & Adair -- [Track 06]. 4 on 6 / Wes Montgomery -- [Track 07]. All of me / Simons and Marks -- [Track 08]. Exactly like you / McHugh & Fields -- [Track 09]. Pent up house / Sonny Rollins -- [Track 10]. Ornithology / Charlie Parker -- [Track 11]. Black Orpheus / Luiz Bonfa -- [Track 12]. Bluesette / Toots Thielemans -- [Track 13]. Asturias / Isaac Albeniz

Mutations in pericentrin cause Seckel syndrome with defective ATR-dependent DNA damage signaling

Large brain size is one of the defining characteristics of modern humans. Seckel syndrome (MIM 210600), a disorder of markedly reduced brain and body size, is associated with defective ATR-dependent DNA damage signaling. Only a single hypomorphic mutation of ATR has been identified in this genetically heterogeneous condition. We now report that mutations in the gene encoding pericentrin (PCNT)--resulting in the loss of pericentrin from the centrosome, where it has key functions anchoring both structural and regulatory proteins--also cause Seckel syndrome. Furthermore, we find that cells of individuals with Seckel syndrome due to mutations in PCNT (PCNT-Seckel) have defects in ATR-dependent checkpoint signaling, providing the first evidence linking a structural centrosomal protein with DNA damage signaling. These findings also suggest that other known microcephaly genes implicated in either DNA repair responses or centrosomal function may act in common developmental pathways determining human brain and body size

Understanding TERT promoter mutations: a common path to immortality

Telomerase (TERT) activation is a fundamental step in tumorigenesis. By maintaining telomere length, telomerase relieves a main barrier on cellular lifespan, enabling limitless proliferation driven by oncogenes. The recently discovered, highly recurrent mutations in the promoter of TERT are found in over 50 cancer types, and are the most common mutation in many cancers. Transcriptional activation of TERT, via promoter mutation or other mechanisms, is the rate-limiting step in production of active telomerase. Although TERT is expressed in stem cells, it is naturally silenced upon differentiation. Thus, the presence of TERT promoter mutations may shed light on whether a particular tumor arose from a stem cell or more differentiated cell type. It is becoming clear that TERT mutations occur early during cellular transformation, and activate the TERT promoter by recruiting transcription factors that do not normally regulate TERT gene expression. This review highlights the fundamental and widespread role of TERT promoter mutations in tumorigenesis, including recent progress on their mechanism of transcriptional activation. These somatic promoter mutations, along with germline variation in the TERT locus also appear to have significant value as biomarkers of patient outcome. Understanding the precise molecular mechanism of TERT activation by promoter mutation and germline variation may inspire novel cancer cell-specific targeted therapies for a large number of cancer patients.Support was provided from a generous gift from the Dabbiere family(RJB,AM,JFC), the Hana Jabsheh Research Initiative (RJB,AM,JFC), and NIH grants NCI P50CA097257 (RJB,AM,JFC), P01CA118816-06 (RJB,AM,JFC), R01HG003008 (HTR), and R01CA163336 (JSS). Additional support was provided from the Sontag Foundation Distinguished Scientist Award (JSS), Fundação para a Ciência e Tecnologia SFRH/BD/88220/2012 (AXM), IF/00601/2012 (BMC), Programa Operacional Regional do Norte (ON.2—O Novo Norte) (BMC), Quadro de Referência Estratégico Nacional (BMC), and Fundo Europeu de Desenvolvimento Regional (BMC).info:eu-repo/semantics/publishedVersio