Stand Up, Speak Out: The Practice and Ethics of Public Speaking

The two key themes to Stand up, Speak out: The Practice and Ethics of Public Speaking make it a welcomed addition to the choices you have for a public speaking textbook. First it focuses on helping students become more seasoned and polished public speakers, and second, its emphasis on ethics in communication. It is this practical approach and integrated ethical coverage that sets Stand up, Speak out: The Practice and Ethics of Public Speaking apart from the other texts in this market. In a world that is bombarded by information, the skills set of public speaking is more important today than ever. According to an address given by Tony Karrer at the TechKnowledge 2009, the New York Times has more information in one week than individuals in the 1800s would encounter in a lifetime. Currently, the amount of information available to people doubles every 18 months and is expected to double weekly by 2015. In a world filled with so much information, knowing how to effectively organize and present one’s ideas through oral communication is paramount. From audience analysis to giving a presentation, Stand up, Speak out: The Practice and Ethics of Public Speaking will guide students through the speech making process. The authors focus on the process of speech making because they have created this book to be a user-friendly guide to creating, researching, and presenting public speeches. While both classic and current academic research in public speaking guide this book, the authors believe that a new textbook in public speaking should first, and foremost, be a practical book that helps students prepare and deliver a variety of different types of speeches — and that is the primary goal of this book. With practicality in mind, the authors developed, Stand up, Speak out: The Practice and Ethics of Public Speaking, as a streamlined public speaking textbook. Many public speaking textbooks today contain over twenty different chapters, which is often impossible to cover in a ten-week quarter or a sixteen-week semester; this textbook is eighteen unique chapters. The fifteen chapters are divided into four clear units of information: introduction to public speaking, speech preparation, speech creation, and speech presentation. In addition to practicality, this text has a focus on the ethics of public speaking from both a source’s and a receiver’s point of view. In 2006 Pearson, Child, Mattern, and Kahl examined the state of ethics in public speaking textbooks. Specifically, the researchers used the NCA Credo on Ethical Communication to guide their study of ethics in public speaking textbooks. Ultimately, the researchers focused on eight specific categories of public speaking ethics content areas: freedom of speech, honesty, plagiarism, ethical listening, ethical research, hate words, diversity, and codes of ethics. As a whole, the top ten public speaking books varied in their degrees of exposure to the various ethical issues. The authors believe that using the NCA Credo on Ethical Communication as the basis for discussing ethics within this book in addition to the latest research in ethics and communication will help students see how ethics can be applied to the public speaking context. All three of the coauthors on this text have conducted research on the topic of communication ethics and written about how ethics is important in every facet of students’ communicative lives. Stand up, Speak out: The Practice and Ethics of Public Speaking, is intended for the one-semester Public Speaking course

Public Speaking: Practice & Ethics

From audience analysis to giving a presentation, Stand Up, Speak Out: The Practice and Ethics of Public Speaking will guide students through the speech-making process. We believe that it is important to focus on the practical process of speech making because we want this book to be a user-friendly guide to creating, researching, and presenting public speeches. While both classic and current academic research in public speaking will guide the book, we do not want to lose the focus of helping students become more seasoned and polished public speakers. We believe that a new textbook in public speaking should first, and foremost, be a practical book that helps students prepare and deliver a variety of different types of speeches

Sex, fat and the tilt of the earth: effects of sex and season on the feeding response to centrally administered leptin in sheep

Whilst there have been many studies in various species examining the effects of leptin on food intake, there is a paucity of data comparing responsiveness in the two sexes. We have, therefore, addressed this issue in sheep. Because this species shows seasonal variation in voluntary food intake (VFI), we also considered the possibility that there might be seasonal variation in the responsivity to leptin. Centrally administered leptin was relatively ineffective as a satiety factor in either sex during AUTUMN: In Spring, leptin had a profound inhibitory effect on VFI in the females, but only a slight effect in males. These data indicate that responsiveness to leptin depends on sex and also on season in animals that are substantially affected by photoperiod

Interaction between p53 mutation and a somatic HDMX biomarker better defines metastatic potential in breast cancer

Abstract TP53 gene mutation is associated with poor prognosis in breast cancer, but additional biomarkers that can further refine the impact of the p53 pathway are needed to achieve clinical utility. In this study, we evaluated a role for the HDMX-S/FL ratio as one such biomarker, based on its association with other suppressor mutations that confer worse prognosis in sarcomas, another type of cancer that is surveilled by p53. We found that HDMX-S/FL ratio interacted with p53 mutational status to significantly improve prognostic capability in patients with breast cancer. This biomarker pair offered prognostic utility that was comparable with a microarray-based prognostic assay. Unexpectedly, the utility tracked independently of DNA-damaging treatments and instead with different tumor metastasis potential. Finally, we obtained evidence that this biomarker pair might identify patients who could benefit from anti-HDM2 strategies to impede metastatic progression. Taken together, our work offers a p53 pathway marker, which both refines our understanding of the impact of p53 activity on prognosis and harbors potential utility as a clinical tool. Cancer Res; 75(4); 698–708. ©2015 AACR.</jats:p

Translation reprogramming is an evolutionarily conserved driver of phenotypic plasticity and therapeutic resistance in melanoma

The intra-tumour microenvironment generates phenotypically distinct but inter-convertible malignant cell subpopulations that fuel metastatic spread and therapeutic-resistance. Whether different microenvironmental cues impose invasive or therapy-resistant phenotypes via a common mechanism is unknown. In melanoma, low expression of the lineage-survival oncogene Microphthalmia-associated transcription factor (MITF) correlates with invasion, senescence and drug-resistance. However, how MITF is suppressed in vivo, and how MITF-low cells in tumors escape senescence is poorly understood. Here we show that microenvironmental cues, including inflammation-mediated resistance to adoptive T-cell immunotherapy, transcriptionally repress MITF via ATF4 in response to inhibition of translation initiation factor eIF2B. ATF4, a key transcription mediator of the integrated stress response, also activates AXL and suppresses senescence to impose the MITF-low, AXL-high drug-resistant phenotype observed in human tumors. However, unexpectedly, without translation reprogramming an ATF4- high, MITF-low state is insufficient to drive invasion. Importantly, translation reprogramming dramatically enhances tumorigenesis and is linked to a previously unexplained gene expression program associated with antiPD-1 immunotherapy resistance. Since we show inhibition of eIF2B also drives neural crest migration and yeast invasiveness, our results suggest that translation reprogramming, an evolutionarily conserved starvation-response, has been hijacked by microenvironmental stress signals in melanoma to drive phenotypic plasticity, invasion and determine therapeutic outcome

Translation reprogramming is an evolutionarily conserved driver of phenotypic plasticity and therapeutic resistance in melanoma.

The intra-tumour microenvironment generates phenotypically distinct but inter-convertible malignant cell subpopulations that fuel metastatic spread and therapeutic-resistance. Whether different microenvironmental cues impose invasive or therapy-resistant phenotypes via a common mechanism is unknown. In melanoma, low expression of the lineage-survival oncogene Microphthalmia-associated transcription factor (MITF) correlates with invasion, senescence and drug-resistance. However, how MITF is suppressed in vivo, and how MITF-low cells in tumors escape senescence is poorly understood. Here we show that microenvironmental cues, including inflammation-mediated resistance to adoptive T-cell immunotherapy, transcriptionally repress MITF via ATF4 in response to inhibition of translation initiation factor eIF2B. ATF4, a key transcription mediator of the integrated stress response, also activates AXL and suppresses senescence to impose the MITF-low, AXL-high drug-resistant phenotype observed in human tumors. However, unexpectedly, without translation reprogramming an ATF4- high, MITF-low state is insufficient to drive invasion. Importantly, translation reprogramming dramatically enhances tumorigenesis and is linked to a previously unexplained gene expression program associated with antiPD-1 immunotherapy resistance. Since we show inhibition of eIF2B also drives neural crest migration and yeast invasiveness, our results suggest that translation reprogramming, an evolutionarily conserved starvation-response, has been hijacked by microenvironmental stress signals in melanoma to drive phenotypic plasticity, invasion and determine therapeutic outcome