The Total Filmmaker: thinking of screenwriting, directing and editing as one role

As screenwriting continues to establish itself as a discrete discipline in academia, either in alignment with creative writing departments or film and media practice departments, there is a danger that such developments may entrench a distancing of the craft from the cinematic form itself and that such a distancing may ultimately reinforce the screenplay's propensity for dramaturgy and the dramatic, rather than the sensory and experiential of the cinematic. Closely related creative stages in telling cinematic stories include directing and editing and this article seeks to argue, with reference to personal screen practice, that screenwriting, directing and editing are, in fact, three variations of the same thing. The article proposes the notion of the Total Filmmaker who embraces all three aspects of the cinematic storyteller. If the ultimate aim is to create a narrative that fully utilises the unique properties of the cinematic form in telling a story, rather than being dominated by the theatricality of dramatically driven classical narratives. How might one explore the relationship between screenwriting, directing and editing? Can an integrated approach to creating the cinematic blueprint change the way we think of pedagogy and screenwriting

A direct D-bar reconstruction algorithm for recovering a complex conductivity in 2-D

A direct reconstruction algorithm for complex conductivities in $W^{2,\infty}(\Omega)$, where $\Omega$ is a bounded, simply connected Lipschitz domain in $\mathbb{R}^2$, is presented. The framework is based on the uniqueness proof by Francini [Inverse Problems 20 2000], but equations relating the Dirichlet-to-Neumann to the scattering transform and the exponentially growing solutions are not present in that work, and are derived here. The algorithm constitutes the first D-bar method for the reconstruction of conductivities and permittivities in two dimensions. Reconstructions of numerically simulated chest phantoms with discontinuities at the organ boundaries are included.Comment: This is an author-created, un-copyedited version of an article accepted for publication in [insert name of journal]. IOP Publishing Ltd is not responsible for any errors or omissions in this version of the manuscript or any version derived from it. The Version of Record is available online at 10.1088/0266-5611/28/9/09500

Ionization of hydrogen and hydrogenic ions by antiprotons

Presented here is a description of the ionization of hydrogen and hydrogenic ions by antiproton-impact, based on very large scale numerical solutions of the time-dependent Schr\"odinger equation in three spatial dimensions and on analysis of the topology of the electronic eigenenergy surfaces in the plane of complex internuclear distance. Comparison is made with other theories and very recent measurements.Comment: RevTex document, 11 pages, 4 Postscript figures are available from the authors, in press Phys. Rev. Let

Response and Resistance to Paradox-Breaking BRAF Inhibitor in Melanomas

FDA-approved BRAF inhibitors produce high response rates and improve overall survival in patients with BRAF V600E/K-mutant melanoma, but are linked to pathologies associated with paradoxical ERK1/2 activation in wild-type BRAF cells. To overcome this limitation, a next-generation paradox-breaking RAF inhibitor (PLX8394) has been designed. Here, we show that by using a quantitative reporter assay, PLX8394 rapidly suppressed ERK1/2 reporter activity and growth of mutant BRAF melanoma xenografts. Ex vivo treatment of xenografts and use of a patient-derived explant system (PDeX) revealed that PLX8394 suppressed ERK1/2 signaling and elicited apoptosis more effectively than the FDA-approved BRAF inhibitor, vemurafenib. Furthermore, PLX8394 was efficacious against vemurafenibresistant BRAF splice variant-expressing tumors and reduced splice variant homodimerization. Importantly, PLX8394 did not induce paradoxical activation of ERK1/2 in wild-type BRAF cell lines or PDeX. Continued in vivo dosing of xenografts with PLX8394 led to the development of acquired resistance via ERK1/2 reactivation through heterogeneous mechanisms; however, resistant cells were found to have differential sensitivity to ERK1/2 inhibitor. These findings highlight the efficacy of a paradox-breaking selective BRAF inhibitor and the use of PDeX system to test the efficacy of therapeutic agents. © 2017 American Association for Cancer Research

The stomach acts as a barrier against Salmonella in pigs fed a meal diet

Finishing pigs fed a coarsely ground meal (CGM) diet showed increased in vitro death rate of Salmonella in the gastric content and a reduced number of enterobacteria in the small intestine and caecum compared with a finely ground and pelleted diet (FGP). The CGM diet resulted moreover in a slower gastric emptying rate, increased the DM content and established a pH-gradient in the stomach. This affected the microbiota in the gastric digesta resulting in more lactic acid bacteria and fewer enterobacteria. Consequently Salmonella bacteria are killed in the stomach and do not enter and proliferate in other parts of the gastrointestinal tract. Furthermore the time after feeding a meal is of importance to whether or not Salmonella bacteria will survive transit through the stomach

Centrosome loss results in an unstable genome and malignant prostate tumors

Localized, nonindolent prostate cancer (PCa) is characterized by large-scale genomic rearrangements, aneuploidy, chromothripsis, and other forms of chromosomal instability (CIN), yet how this occurs remains unclear. A well-established mechanism of CIN is the overproduction of centrosomes, which promotes tumorigenesis in various mouse models. Therefore, we developed a single-cell assay for quantifying centrosomes in human prostate tissue. Surprisingly, centrosome loss-which has not been described in human cancer-was associated with PCa progression. By chemically or genetically inducing centrosome loss in nontumorigenic prostate epithelial cells, mitotic errors ensued, producing aneuploid, and multinucleated cells. Strikingly, transient or chronic centrosome loss transformed prostate epithelial cells, which produced highly proliferative and poorly differentiated malignant tumors in mice. Our findings suggest that centrosome loss could create a cellular crisis with oncogenic potential in prostate epithelial cells.6 month embargo; published online: 2 September 2019This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]