How to Choose the Perfect Font for Any Situation. Ever have one of those days where you’re just sitting around, falsifying documents, and just can’t seem to choose the right font to convey your alleged corruption? 3D Cell Simulation and Stain Tool – Learn about the cell and its structures in a 3D tool; 3D Heart & Circulatory Premium – An amazingly detailed App that shows. Ever have one of those days where you’re just sitting around, falsifying documents, and just can’t seem to choose the right font to convey your alleged corruption? It’s cool. We’ve all been there. But how often—be real—do you think about the font you’re using?
You’re exposed to words in all shapes and sizes on a daily basis, whether texting a friend, writing a resumé, or jotting notes in your text editor of choice. But fonts convey different meanings, and if you pick the wrong one you could find yourself either dismissed for a potential job opportunity, or worse, laughed at by everyone in the office before they throw your résumé in the trash. You Can Do Better Than Times New Roman. Everyone uses Times New Roman. It’s the default font for every standard resume, book report, term paper, and any other official missive you can recall. Sure, it looks stately, but it also looks boring, and implies a lack of intentionality. Instead, pick a similarly styled font like Garamond or Charter to show you both care about readability as well as style. Depending on the size of your Mac’s screen, the font in Finder windows can be awfully small and…Read more You Can’t Go Wrong With Helvetica. You know it, you love it, you can’t live without it, it’s Helvetica! The font synonymous with great design is always a good choice if you’re not sure how to proceed with your pick of typeface. It feels professional, lighthearted, honest,” Brian Hoff of Brian Hoff Design told Bloomberg. The sans- serif font is modern, weighted evenly, and used in everything from Fortune 1. MTA’s subway system. Unfortunately, if you’re a Windows user you’ll have to actually purchase the font yourself: Microsoft created its own Helvetica clone, Arial, as it chose not to license the famous font. In the words of Cleaver Magazine editor Remy Barnes, “For the love of God, do not send Arial.”Use Thicker Fonts for Reading on Screens. While some fonts, like Baskerville, are great for long reads on paper, they’re harder to read on devices with low resolution screens. Poor screen quality means poor rendering of the font’s thinnest lines, making reading more of a challenge. Use thicker fonts like Palatino and Georgia, which are better suited for screen reading, according to font designer and retired professor Charles Bigelow. Stop With the Comic Sans Already. Under no circumstances, unless you’re 8, should you use Comic Sans. Its original purpose was to act as the text for speech bubbles in Microsoft Word. Since its creation in ’9. Please license Helvetica, Microsoft.
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It's a busy week again here at Casa MetroDad. Work is busy. My MIL is in town. And Lord knows my DVR is bursting at the seams. Therefore, posting may be a little light. Lyberty.com's weekly/monthly splash page. (Yes, a splash page is old fashioned, but it's been a tradition here since 1999.). Volkswagen RNS 510 Firmware Download Repository We strongly recommend that you read the details page prior to downloading and upgrading firmware for specific. This is a great condition used VW RNS-510 Navigation. Part number is 3C0 035 684B. It comes with the security code, SW:1140, the latest V11 maps, and Video in Motion. Upgrading 2nd generation headunits (RCD 300, RCD 500, MFD2) to 3rd generation headunits (RCD 210, RCD 310, RNS 310, RNS 510, RCD 510). Find contact details for Harrogate Volkswagen Volkswagen. Discover our range of VW cars and services on offer today. Offers 50 GB of free storage space. Uploaded files are encrypted and only the user holds the decryption keys. 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Lecturer: Peter Sorger, Harvard Medical School, Boston, MA. The development of new therapeutic drugs is fundamental to improving human health, but the process is challenged by rising costs and a high rate of failure. New and better technology and big data are often put forward as the solutions to these problems. However, I will discuss laboratory and clinical studies showing that some of the fundamental concepts in pharmacology and toxicology are ripe for reinvention. Increasing data on the impact of cell- to- cell variability and temporal variation in cellular physiology motivates new ways of thinking about seemingly simple concepts such as drug dose- response. Better understanding of sources of variation in laboratory and clinical data should also improve our ability to identify robust biomarkers of therapeutic and adverse effects. I will argue that big data and data science are essential but insufficient: correct interpretation of empirical data in biomedicine hinges on theories about mechanism. I will discuss these theories, with reference to cytotoxic and targeted anti- cancer therapies, and studies of drug response in cell culture, animal models, and human clinical trials. New pharmacological principles derived from such studies are being developed into practical algorithms and open- source software as a means to improve target qualification, lead molecule optimization, and early phase clinical trials. The hoped for outcome: better drugs at a cost society can afford. Open Ecosystems for Understanding Toxicities and Adverse Events. Lecturer: Lara Mangravite, Sage Bionetworks, Seattle, WA. The presentation will address the use of collaborative approaches for the gathering, sharing and interpretation of health data. This will include the use of remote sensor- based data collection approaches to capture fluctuations in health relative to medication and disease—and the consideration of how these could be used to track adverse events. Merit Award Lecture. Monday, March 1. 3, 1. PM to 1: 2. 0 PMCell Proliferation and Carcinogenesis: Bad Luck and the Environment. Lecturer: Samuel M. Cohen, University of Nebraska Medical Center, Omaha, NE. Cancer develops because of multiple permanent genetic errors arising in a single stem cell, a clonal disease. Every time DNA replicates, spontaneous mistakes can occur. Thus, the risk of cancer can be increased by either directly damaging DNA each time it replicates (DNA reactive) or increasing the number of DNA replications (cell proliferation), or both. Some have indicated that the “spontaneous” errors that occur during DNA replication are the basis for cancer being due to “bad luck,” and are the cause of most cancers. However, it is well- known that numerous environmental factors can increase the risk of cancer. This dilemma is readily resolved by realizing that the number of stem cells and the rate of their proliferation can be markedly influenced by the environment. Over the course of more than a 5. I have been actively involved in research on DNA reactive carcinogens (nitrofurans, aromatic amines, nitrosamines) and non- DNA reactive carcinogens (saccharin, PPARγ agonists, arsenicals, others). Based on the fundamentals of carcinogenesis, a mode of action (MOA) approach, and the accumulated knowledge of carcinogenesis in animals and humans, carcinogenic risk can be readily evaluated today without utilizing the two- year bioassay. Meet the Directors: A Conversation with Linda S. Birnbaum and Robert J. Kavlock. Monday, March 1. PM to 2: 3. 0 PMChairperson(s): Patricia E. Ganey, Society of Toxicology Vice President; Michigan State University, East Lansing, MI. Panelists: Linda S. Birnbaum, NIEHS, Research Triangle Park, NC; and Robert J. Kavlock, US EPA, Washington, DC. This important session will provide an informal venue for meeting attendees to have a candid and open discussion with two key leaders of federal organizations with missions to protect and improve public health: Dr. Birnbaum, Director, National Institute of Environmental Health Sciences (NIEHS), NIH, and Dr. Kavlock, Deputy Assistant Administrator for Science at the Office of Research and Development for the US EPA. The entire session will be devoted to a question- and- answer format concerning scientific directions and priorities for NIEHS and EPA including funding priorities and outlooks, and training opportunities. SOT/EUROTOX Debate. Monday, March 1. 3, 4: 4. PM to 6: 0. 0 PMToxicology Testing of Drug Combinations Does Not Add Significant Value to Human Risk Evaluation Beyond What Is Known for the Individual Agents. Chairperson(s): Leigh Ann Burns Naas, Gilead Sciences Inc., Foster City, CA; and Heather Wallace, University of Aberdeen, Aberdeen, United Kingdom. SOT Debater: Kenneth L. Hastings, Hastings Toxicology Consulting LLC, Mount Airy, MD. EUROTOX Debater: Phil Bentley, Toxicodynamix International LLC, Hendersonville, NC, and Basel, Switzerland. Endorser(s): Society of Toxicology (SOT)European Societies of Toxicology (EUROTOX)Each year the SOT Annual Meeting includes a debate that continues a tradition that originated in the early 1. This year, our debaters will address the proposition: Toxicology Testing of Drug Combinations Does Not Add Significant Value to Human Risk Evaluation Beyond What is Known for the Individual Agents. The use of innovative drug combinations—both large and small molecule—in clinical development is increasing. The objective is often to increase efficacy by targeting multiple pathways for the same disease, to improve safety by being able to lower doses of one or more drugs, or to provide more convenient/acceptable therapies to patients. As the number of these clinical combinations rises, there is an increasing need to evaluate their nonclinical safety. At the heart of this evaluation is the question regarding the need for actual animal testing. Global regulatory guidance has provided a framework for the nonclinical safety evaluation of combination products, which considers the need for testing based on such things as the potential for PK or PD interactions, overlapping toxicology profiles, extent of toxicology characterization of the individual agents and their margins of safety, human clinical experience with the individual agents, and the stage of clinical development of each agent. The guidance applies not only to fixed dose combinations but co- packaged and co- use as well. Unless there is clinical experience with the combination and that combination involves two late stage (Phase 3, Marketed) entities, nonclinical repeat dose toxicity studies up to 9. This broad recommendation is inconsistent with the principles of the 3. Rs for reduction, refinement, and replacement in animal experimentation. Conversely, the potential for unexpected safety events with novel, targeted therapies is a clear clinical concern. The debaters will discuss the evidence regarding whether the information gathered in nonclinical combination studies provides clear benefit in the overall risk evaluation for clinical combinations. Regardless of framework differences and personal convictions, each scientific debate delegate will present relevant evidence and compelling scientific arguments to persuade and appeal to the audience in order to obtain the approval or rejection of the motion. In addition to being a featured session at the SOT Annual Meeting in Baltimore, Maryland, this debate will again take place (with the debaters taking the reverse positions) in Bratislava, Slovak Republic, during the 5. Congress of the European Societies of Toxicology (2. EUROTOX Annual Congress), September 1. Daily Plenary Session: Precision Medicine. Tuesday, March 1. AM to 9: 2. 0 AMView this Plenary Presentation Pharmacogenomics of Drug Toxicity in Cancer: Making the Case for Precision Medicine. Lecturer: Jun J. Yang, St. Jude Children’s Research Hospital, Memphis, TN. Elucidation of the genetic basis for inter- patient variability in drug toxicity not only reveals important biology of a drug’s mechanism of action but also provides critical knowledge that enables risk- adapted treatment individualization. This is particularly relevant in cancer where chemotherapy is often associated with severe acute toxicities and debilitating long- term side effects. Therefore, the narrow therapeutic index of anti- leukemic drugs provides a compelling rationale for improvements in evidence- based precision medicine approaches. Focusing on acute lymphoblastic leukemia as a model disease, our pharmacogenomics research identifies genetic factors associated with response and toxicity of a wide range of common anti- cancer drugs, from which we then develop genetics- guided individualized therapy. For example, inherited deficiency in detoxification enzymes TPMT and NUDT1. In fact, there is a rapidly- growing number of medications for which pharmacogenomic variants can directly guide treatment choice and/or dosing strategy. At the forefront of precision medicine, pharmacogenomics hold particularly great promise to transform medical practice with more efficacious and safer therapies across diseases. The Role of Precision Medicine in Closing the Innovation Gap. Lecturer: Richard Barker, University of Oxford, Oxford, United Kingdom. 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