1,057 research outputs found
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Shabbat B'shir
No full textShabbat B’shir is an album exploring Jewish folk and rock music written, performed, produced, recorded, and mixed and mastered all by Max Winer. The goal of the project was to create a full length album showcasing Max Winer’s growth in songwriting and production capabilities. This eleven song album features the liturgy of the Kabbalat Shabbat (Friday night) Jewish worship service. This paper outlines the creation and production of Shabbat B’shir, including: the conception of the project; it’s connection to the modern Jewish library of music; the creation of the album; the recording methodology; the engineering process; the mixing and mastering process; and the learning outcomes/expectations.
Key Words: Music, Sacred Music, Judaism, Jewish Music, Music Productio
Replacing safe havens with a safe system
No full textArticle based on a presentation given at the Sixteenth International Symposium on Economic Crime by Jonathan Winer (Deputy Assistant Secretary of State, Narcotics & Law Enforcement). The author analyses the background to worldwide financial services collapses. Published as part of a Symposium report in Amicus Curiae - Journal of the Institute of Advanced Legal Studies and its Society for Advanced Legal Studies. The Journal is produced by the Society for Advanced Legal Studies at the Institute of Advanced Legal Studies, University of London
Replacing safe havens with a safe system
No full textArticle based on a presentation given at the Sixteenth International Symposium on Economic Crime by Jonathan Winer (Deputy Assistant Secretary of State, Narcotics & Law Enforcement). The author analyses the background to worldwide financial services collapses. Published as part of a Symposium report in Amicus Curiae - Journal of the Institute of Advanced Legal Studies and its Society for Advanced Legal Studies. The Journal is produced by the Society for Advanced Legal Studies at the Institute of Advanced Legal Studies, University of London
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Long-term hepatitis B infection in a scalable hepatic co-culture system.
No full textVolume 8, Issue 1, 1 December 2017, Article number 125, pgs. 1-11. Authors: Benjamin Y. Winer, Tiffany S. Huang, Eitan Pludwinski, Brigitte Heller, Felix Wojcik, Gabriel E. Lipkowitz, Amit Parekh, Cheul Cho, Anil Shrirao, Thomas W. Muir (Tom W. Muir), Eric Novik & Alexander Ploss.Hepatitis B virus causes chronic infections in 250 million people worldwide. Chronic hepatitis B virus carriers are at risk of developing fibrosis, cirrhosis, and hepatocellular carcinoma. A prophylactic vaccine exists and currently available antivirals can suppress but rarely cure chronic infections. The study of hepatitis B virus and development of curative antivirals are hampered by a scarcity of models that mimic infection in a physiologically relevant, cellular context. Here, we show that cell-culture and patient-derived hepatitis B virus can establish persistent infection for over 30 days in a self-assembling, primary hepatocyte co-culture system. Importantly, infection can be established without antiviral immune suppression, and susceptibility is not donor dependent. The platform is scalable to microwell formats, and we provide proof-of-concept for its use in testing entry inhibitors and antiviral compounds.The lack of models that mimic hepatitis B virus (HBV) infection in a physiologically relevant context has hampered drug development. Here, Winer et al. establish a self-assembling, primary hepatocyte co-culture system that can be infected with patient-derived HBV without further modifications
Triple-negative breast cancer: disease entity or title of convenience?
No full textThis Review outlines the understanding and management of triple-negative breast cancer (TNBC). TNBC shares morphological and genetic abnormalities with basal-like breast cancer (BLBC), a subgroup of breast cancer defined by gene-expression profiling. However, TNBC and BLBC tumors are heterogeneous and overlap is incomplete. Breast cancers found in BRCA1 mutation carriers are also frequently triple negative and basal like. TNBC and BLBC occur most frequently in young women, especially African Americans, and tend to exhibit aggressive, metastatic behavior. These tumors respond to conventional chemotherapy but relapse more frequently than hormone receptor-positive, luminal subtypes and have a worse prognosis. New systemic therapies are urgently needed as most patients with TNBC and/or BLBC relapse with distant metastases, and hormonal therapies and HER2-targeted agents are ineffective in this group of tumors. Poly (ADP-ribose) polymerase inhibitors, angiogenesis inhibitors, EGFR-targeted agents, and src kinase and mTOR inhibitors are among the therapeutic agents being actively investigated in clinical trials in patients with TNBC and/or BRCA1-associated tumors. Increased understanding of the genetic abnormalities involved in the pathogenesis of TNBC, BLBC and BRCA1-associated tumors is opening up new therapeutic possibilities for these hard-to-treat breast cancers
Social Welfare and Coercion in Public Finance
No full textThis paper develops an expanded framework for social planning in which the existence of coercion is explicitly acknowledged. Key issues concern the precise definition of coercion for individuals and in the aggregate, its difference from redistribution, and its incorporation into normative analysis. We explore modifications to traditional rules for optimal fiscal policy in the presence of coercion constraints and determine the degree of coercion implied by traditional social planning. The paper maps the trade-off between social welfare and aggregate coercion and explores its implications for normative policy and the comparative evaluation of institutions, including competitive democracy.coercion, redistribution, social planning, optimal fiscal policy, marginal cost of funds, public goods, collective choice
Cardiac toxicity from systemic cancer therapy : a comprehensive review
No full textCardiovascular toxicity is a potential short- or long-term complication of anticancer therapy. Exposure to chemotherapy medications, primarily the anthracycline class, can lead to potentially irreversible clinically significant cardiac dysfunction. The advent of novel biologic agents, including monoclonal antibodies and tyrosine kinase inhibitors, has revolutionized the treatment of several types of malignancies. Although targeted therapies are considered less toxic and better tolerated by patients compared with classic chemotherapy agents, rare serious complications have been observed; and longer-term follow-up is needed to determine the exact profile of related cardiac adverse effects. Cardiac toxicity associated with cancer therapies can range from asymptomatic subclinical abnormalities, including electrocardiographic changes and temporary left ventricular ejection fraction decline, to life-threatening events such as congestive heart failure or acute coronary syndromes. Assessment of the prevalence, type, and severity of cardiac toxicity caused by various cancer treatments is a critical topic for patient management and specifically for new drug development. Guidelines for monitoring cardiac adverse effects have been formulated; however, appropriate supportive evidence remains limited. Given the rate of new drug development designed to fulfill unmet oncologic needs, efforts are needed to promote strategies for cardiac risk detection and management and to avoid unintended consequences potentially impeding development of, regulatory approval for, and patient access to novel therapies. These advances require ongoing research to assess and manage the cardiovascular safety of patients treated with anticancer agents, as well as a well-organized collaboration between oncologists and cardiologists. The aim of this review is to summarize potential cardiovascular toxicities for a range of cancer chemotherapeutics and to review general mechanisms of cardiovascular toxicity for each agent
Analysis of beta-catenin's amino-terminal domain and ITF -2, a beta-catenin/TCF-regulated gene, in neoplastic transformation.
No full textThe WNT signaling pathway is essential for proliferation, differentiation and morphogenesis. In the canonical pathway, WNTs bind to their receptors and stabilize the beta-catenin protein ultimately allowing its translocation to the nucleus. There, beta-catenin binds to members of the T-Cell Factor (TCF) family and activates, or represses, the transcription of target genes. Mutagenesis screening was utilized to identify mutations in beta-catenin's amino-terminal region that lead to neoplastic transformation of epithelial cells. The screen identified a number of mutations in the GSK-3beta phosphorylation domain of beta-catenin. Directed mutagenesis identified two lysine residues (K19 and K49) outside of this domain. The K19/K49 double mutation dramatically decreased the ubiquitination of beta-catenin, stabilizing the transcriptionally active fractions (i.e. the cytoplasmic free pool and nuclear beta-catenin fractions) and increasing beta-catenin's ability to promote neoplastic transformation. Studies of downstream targets of the WNT pathway have highlighted how defects in the pathway contribute to cancer. We found that Immunoglobulin Transcription Factor 2 (ITF-2), a class I bHLH protein, was directly upregulated in beta-catenin transformed cells and responded to WNT signaling perturbations in human cancer cell lines. Upstream elements in the promoter of ITF-2 also responded to TCF/beta-catenin mediated signaling. ITF-2 protein levels were upregulated in many cancers, often associated with increased nuclear beta-catenin. Finally, studies of ITF-2 in APCMIN mouse intestinal tumorigenesis suggest that ITF-2 may play a vital role in tumorigenesis. The explosion of data surrounding WNT signaling in development and disease has painted a detailed picture, while yielding more questions for the future. The regulation of beta-catenin via structural domains and their effects on localization, binding of cofactors and downstream signal transduction needs to be addressed. The end result of this cascade is upregulation (or downregulation) of target genes. The challenge that lies ahead is identification of critical targets and translation of this knowledge to interventions that specifically target the disease state while maintaining the wide range of normal functions of the pathway which are critical to survival.PhDBiological SciencesHealth and Environmental SciencesImmunologyMolecular biologyUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/126591/2/3253432.pd
Democracy, Inequality and the Environment when Citizens can Mitigate Privately or Act Collectively
No full textWe study the political economy of the environment in autocratic, weak and strong democracies when individuals can either mitigate the health consequences of domestic pollution privately or reduce pollution collectively through public policy. The setting is that of a small open economy in which incomes depend importantly on trade in dirty goods, where income inequality and the degree to which ordinary citizens exert voice in each dimension of the policy process distinguishes elites and ordinary citizens. The recognition that the health consequences of pollution can be dealt with privately at a cost adds an important dimension to the analysis of the political economy of environmental regulation, especially for an open economy. When private mitigation is feasible, inequality of incomes leads to an unequal distribution of the health burden of pollution (in accordance with the epidemiologic evidence), thus polarizing the interests of citizens in democracies and of ordinary citizens and elites in non-democratic regimes. Inequality in the willingness to bear the cost of private mitigation in turn interacts with the pollution costs and income benefits of trade in dirty goods to further polarize interests concerning both environmental stringency and the regulation of trade openness. In this context, we show how the eco-friendliness ranking of different political regimes varies with the cost of private mitigation and with the extent of income inequality, tending to converge when mitigation costs are high, and even producing a ranking reversal between democracies and autocracies, and between weak and strong democracies, when costs lie in an intermediate range.pollution, environmental regulation, private mitigation, income inequality, democracy, trade, welfare, collective choice, political economy
Does grit protect against the adverse effects of depression?
No full textGrit, or the ability to persevere toward a long-term goal despite adversity, has been linked to academic success. Grit may also potentially buffer against the negative effects of depressive symptoms in an academic domain. The current study explores the relationship between depression, grit, and GPA, while also accounting for defensive responding, which has been proposed as a confound of grit but not empirically assessed in this context. We examined how social desirability affects the relationship between grit and GPA and hypothesized that social desirability would moderate the effect of grit between depressive symptoms and GPA. We found support for all hypothesized direct relationships. However, the interaction between depression, grit, social desirability, and GPA was non-significant. Results suggested modest construct validity of grit with it predicting GPA at low levels of social desirability but demonstrated no buffering effect against depression on GPA, highlighting the complexity of the relationship between these variables
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