A host of factors regulating influenza virus replication.

A new series of genetic screens begins to illuminate the interaction between influenza virus and the infected cell

More in Defense of Weak Scientism

In my (2017a), I defend a view I call Weak Scientism, which is the view that knowledge produced by scientific disciplines is better than knowledge produced by non-scientific disciplines. Scientific knowledge can be said to be quantitatively better than non-scientific knowledge insofar as scientific disciplines produce more impactful knowledge–in the form of scholarly publications–than non-scientific disciplines (as measured by research output and research impact). Scientific knowledge can be said to be qualitatively better than non-scientific knowledge insofar as such knowledge is explanatorily, instrumentally, and predictively more successful than non-scientific knowledge. Brown (2017a) raises several objections against my defense of Weak Scientism and I have replied to his objections (Mizrahi 2017b), thereby showing again that Weak Scientism is a defensible view. Since then, Brown (2017b) has reiterated his objections in another reply on SERRC. In this paper, I respond to Brown's objections, thereby showing once more that Weak Scientism is a defensible view

Informal Fallacies in Legal Argumentation

Article published in the South Carolina Law Review

Safe Harbor for Officer Reliance: Comparing the Approaches of the Model Business Corporation Act and Delaware’s General Corporation Law

Balotti and Shaner discuss the duties of and potential for imposing liability on corporate officers. The fiduciary duties of officers is addressed, in differing degrees, under Delaware law, the law frequently applied to corporate-governance disputes, and under the Model Business Corporation Act (MBCA). In discharging their fiduciary duties, directors under both the MBCA and the General Corporation Law are generally protected from personal liability if, in making business decisions, they reasonably rely on the reports and records of officers, employees, advisors, and experts of the corporation

Matthew Lipman: testimonies and homages

We lead off this issue of Childhood and Philosophy with a collection of testimonies, homages, and brief memoirs offered from around the world in response to the death of the founder of Philosophy for Children, Matthew Lipman on December 26, 2010, at the age of 87. To characterize Lipman as “founder” is completely accurate, but barely evokes the role he played in conceiving, giving birth to, and nurturing this curriculum cum pedagogy that became a movement, and which has taken root in over 40 countries, from Iceland to Nigeria to Taiwan to Chile and everywhere in between. The movement itself is broader than the program, which has in fact experienced multiple transformations in multiple contexts over its half-century of life. In fact, as many of the testimonies below either state outright or imply, the movement is an emancipatory one and thus implicitly political, infused with all the long-suffering hope for our species inspired in us by the fact of natality, and by our own intuitive faith in the transformative power of reason—or as Lipman came to call it, “reasonableness.” For those seized by its educational possibilities, it presents a sudden influx of sunlight and fresh air into an institution long stultified by its own rigid habitus, and promises the reconstruction of schooling in the image of authentic democratic practice that recognizes and honors the unique capacities of children. As Philosophy in the Classroom—Lipman’s first and now classic statement of educational philosophy--puts it, the movement promises a re-orientation of the goal of education from information (or “learning”) to meaning, and inaugurates the dialogue with childhood and children that follows from that. Lipman was not just founder of this movement but creator, inventor, developer, convener, organizer, faithful soldier, ambassador, apologist, polemicist, propagandist, and, finally, undying optimist

Host Cell Functions In Vesicular Stomatitis Virus Replication

Vesicular stomatitis virus (VSV), the prototypic rhabdovirus, has been used as an excellent paradigm for understanding the mechanisms of virus replication, pathogenesis, host response to virus infection and also for myriads of studies on cellular and molecular biology. Biochemical studies as well as high-throughput genomics, proteomics, and chemical approaches have revealed a plethora of cellular factors and pathways that regulate replication of VSV. These factors include those that support virus replication and also those that restrict its replication. This chapter discusses the role(s) of many of these host cell factors and pathways involved in VSV replication. Although mechanistic understanding of the roles of some of these factors in VSV replication has been obtained, the roles of many others need to be investigated for a better understanding of the virus-host cell interactions

Sweep-synchronized positionable trigger and supplementary components

This report describes the Sweep-Synchronized Positionable Trigger, together with its functions and supplementary components, as designed and built for use with the Precision Graphic Recorder (PGR) at the Woods Hole Oceanographic Institution. The positionable trigger provides a means for plotting a variable on the PGR record as a function of time, for triggering equipment such as oscilloscopes at any time, for displaying ship's heading, and for supplying, semi-automatically, ocean depth to a ship- board computer.The Office of Naval Research under Contract Nonr- 40 29(00

Host Cell Functions In Vesicular Stomatitis Virus Replication

Vesicular stomatitis virus (VSV), the prototypic rhabdovirus, has been used as an excellent paradigm for understanding the mechanisms of virus replication, pathogenesis, host response to virus infection and also for myriads of studies on cellular and molecular biology. Biochemical studies as well as high-throughput genomics, proteomics, and chemical approaches have revealed a plethora of cellular factors and pathways that regulate replication of VSV. These factors include those that support virus replication and also those that restrict its replication. This chapter discusses the role(s) of many of these host cell factors and pathways involved in VSV replication. Although mechanistic understanding of the roles of some of these factors in VSV replication has been obtained, the roles of many others need to be investigated for a better understanding of the virus-host cell interactions

Endomembrane Trafficking in Plants

The functional organization of eukaryotic cells requires the exchange of proteins, lipids, and polysaccharides between membrane compartments through transport intermediates. Small GTPases largely control membrane traffic, which is essential for the survival of all eukaryotes. Transport from one compartment of this pathway to another is mediated by vesicular carriers, which are formed by the controlled assembly of coat protein complexes (COPs) on donor organelles. The activation of small GTPases is essential for vesicle formation from a donor membrane. In eukaryotic cells, small GTP-binding proteins comprise the largest family of signaling proteins. The ADP-ribosylation factor 1 (ARF1) and secretion-associated RAS superfamily 1 (SAR1) GTP-binding proteins are involved in the formation and budding of vesicles throughout plant endomembrane systems. ARF1 has been shown to play a critical role in coat protein complex I (COPI)-mediated retrograde trafficking in eukaryotic systems, whereas SAR1 GTPases are involved in intracellular coat protein complex II (COPII)-mediated protein trafficking from the endoplasmic reticulum (ER) to the Golgi apparatus. The dysfunction of the endomembrane system can affect signal transduction, plant development, and defense. This chapter offers a summary of membrane trafficking system with an emphasis on the role of GTPases especially ARF1, SAR1, and RAB, their regulatory proteins, and interaction with endomembrane compartments. The vacuolar and endocytic trafficking are presented to enhance our understanding of plant development and immunity in plants