Intercultural Transfer and Balinese Gamelan Preservation

The influence and spread of traditional Balinese music over time and across regions has been conducted through a number of different channels. In addition to locally-focused efforts, cultural transfer has also contributed to the preservation of traditional Balinese arts. From the self-interested, strategic support of gamelan music by Japanese occupational forces to the global experimental music scene today, Balinese arts have been shared, supported, translated, and appropriated in various ways by a number of different actors to political, artistic, and commercial ends. Building on Michel Espagne’s definition of cultural transfer and Stephen Greenblatt’s concept of cultural mobility, this paper aims to outline different modes of cultural transfer (or “bridges,” as Espagne would say), with explicit attention to power dynamics and multi-way flows of influence. Several key historical and contemporary examples of the transfer of traditional Balinese music will be discussed in an effort to better understand the relationship between cultural transfer and preservation

Comparison of the generic neuronal differentiation and neuron subtype specification functions of mammalian achaete-scute and atonal homologs in cultured neural progenitor cells

In the vertebrate peripheral nervous system, the proneural genes neurogenin 1 and neurogenin 2 (Ngn1 and Ngn2), and Mash1 are required for sensory and autonomic neurogenesis, respectively. In cultures of neural tube-derived, primitive PNS progenitors NGNs promote expression of sensory markers and MASH1 that of autonomic markers. These effects do not simply reflect enhanced neuronal differentiation, suggesting that both bHLH factors also specify neuronal identity like their Drosophila counterparts. At high concentrations of BMP2 or in neural crest stem cells (NCSCs), however, NGNs like MASH1 promote only autonomic marker expression. These data suggest that that the identity specification function of NGNs is more sensitive to context than is that of MASH1. In NCSCs, MASH1 is more sensitive to Notch-mediated inhibition of neurogenesis and cell cycle arrest, than are the NGNs. Thus, the two proneural genes differ in other functional properties besides the neuron subtype identities they can promote. These properties may explain cellular differences between MASH1- and NGN-dependent lineages in the timing of neuronal differentiation and cell cycle exit

Isolation and Profiling of Circulating Tumorâ Associated Exosomes Using Extracellular Vesicular Lipidâ Protein Binding Affinity Based Microfluidic Device

Extracellular vesicles (EVs) are emerging as a potential diagnostic test for cancer. Owing to the recent advances in microfluidics, onâ chip EV isolation is showing promise with respect to improved recovery rates, smaller necessary sample volumes, and shorter processing times than ultracentrifugation. Immunoaffinityâ based microfluidic EV isolation using antiâ CD63 is widely used; however, antiâ CD63 is not specific to cancerâ EVs, and some cancers secrete EVs with low expression of CD63. Alternatively, phosphatidylserine (PS), usually expressed in the inner leaflet of the lipid bilayer of the cells, is shown to be expressed on the outer surface of cancerâ associated EVs. A new exosome isolation microfluidic device (newExoChip), conjugated with a PSâ specific protein, to isolate cancerâ associated exosomes from plasma, is presented. The device achieves 90% capture efficiency for cancer cell exosomes compared to 38% for healthy exosomes and isolates 35% more A549â derived exosomes than an antiâ CD63â conjugated device. Immobilized exosomes are then easily released using Ca2+ chelation. The recovered exosomes from clinical samples are characterized by electron microscopy and westernâ blot analysis, revealing exosomal shapes and exosomal protein expressions. The newExoChip facilitates the isolation of a specific subset of exosomes, allowing the exploration of the undiscovered roles of exosomes in cancer progression and metastasis.Onâ chip exosome isolation using immunoaffinity capture improves recovery from small sample volumes compared to ultracentrifugation. However, tetraspanins are not specific to cancer exosomes and some cancers secrete exosomes with low expression of tetraspanins. Here, a microfluidicâ device conjugated with proteins against phosphatidylserine (PS), shown to be expressed on the outer surface of cancerâ associated exosome, is used to isolate cancerâ associated exosomes.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/152534/1/smll201903600-sup-0001-SuppMat.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/152534/2/smll201903600_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/152534/3/smll201903600.pd

A Data-Driven Computational Model for Engineered Cardiac Microtissues

Engineered heart tissues (EHTs) present a potential solution to some of the current challenges in the treatment of heart disease; however, the development of mature, adult-like cardiac tissues remains elusive. Mechanical stimuli have been observed to improve whole-tissue function and cardiomyocyte (CM) maturation, although our ability to fully utilize these mechanisms is hampered, in part, by our incomplete understanding of the mechanobiology of EHTs. In this work, we leverage the experimental data produced by a mechanically tunable experimental setup to generate tissue-specific computational models of EHTs. Using imaging and functional data, our modeling pipeline generates models with tissue-specific ECM and myofibril structure, allowing us to estimate CM active stress. We use this experimental and modeling pipeline to study different mechanical environments, where we contrast the force output of the tissue with the computed active stress of CMs. We show that the significant differences in measured experimental forces can largely be explained by the levels of myofibril formation achieved by the CMs in the distinct mechanical environments, with active stress showing more muted variations across conditions. The presented model also enables us to dissect the relative contributions of myofibrils and extracellular matrix to tissue force output, a task difficult to address experimentally. These results highlight the importance of tissue-specific modeling to augment EHT experiments, providing deeper insights into the mechanobiology driving EHT function.Comment: 19 pages, 7 figure

Mitochondrial pathology in progressive cerebellar ataxia.

BACKGROUND: Mitochondrial disease can manifest as multi-organ disorder, often with neurological dysfunction. Cerebellar ataxia in isolation or in combination with other features can result from mitochondrial disease yet genetic testing using blood DNA is not sufficient to exclude this as a cause of ataxia. Muscle biopsy is a useful diagnostic tool for patients with ataxia suspected of mitochondrial disease. Our aim was to determine specific patient selection criteria for muscle biopsy to see how frequent mitochondrial mutations are responsible for progressive ataxia. We performed a two centre retrospective review of patients with unexplained progressive ataxia who underwent muscle biopsy for suspected mitochondrial disease between 2004 and 2014 (Sheffield and Newcastle Ataxia Centres). RESULTS: A total of 126 patients were identified; 26 assessed in Newcastle and 100 in Sheffield. Twenty-four patients had pure ataxia and 102 had ataxia with additional features. The total number of patients with histologically suspected and/or genetically confirmed mitochondrial disease was 29/126 (23 %). CONCLUSIONS: A large proportion of patients (23 %) with progressive ataxia who underwent muscle biopsy were found to have features of mitochondrial dysfunction, with molecular confirmation in some. Muscle biopsy is a helpful diagnostic tool for mitochondrial disease in patients with progressive ataxia

Recruitment of Pontin/Reptin by E2f1 amplifies E2f transcriptional response during cancer progression

Changes in gene expression during tumorigenesis are often considered the consequence of de novo mutations occurring in the tumour. An alternative possibility is that the transcriptional response of oncogenic transcription factors evolves during tumorigenesis. Here we show that aberrant E2f activity, following inactivation of the Rb gene family in a mouse model of liver cancer, initially activates a robust gene expression programme associated with the cell cycle. Slowly accumulating E2f1 progressively recruits a Pontin/Reptin complex to open the chromatin conformation at E2f target genes and amplifies the E2f transcriptional response. This mechanism enhances the E2f-mediated transactivation of cell cycle genes and initiates the activation of low binding affinity E2f target genes that regulate non-cell-cycle functions, such as the Warburg effect. These data indicate that both the physiological and the oncogenic activities of E2f result in distinct transcriptional responses, which could be exploited to target E2f oncogenic activity for therapy