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61 result(s) for "Monk, Simon"
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From Cards to Code: How Extreme Programming Re-Embodies Programming as a Collective Practice
This paper discusses Extreme Programming (XP), a relatively new and increasingly popular ‘user-centred’ software design approach. Extreme Programming proposes that collaborative software development should be centred on the practices of programming. That proposal contrasts strongly with more heavily instrumented, formalised and centrally managed software engineering methodologies. The paper maps the interactions of an Extreme Programming team involved in building a commercial organisational knowledge management system. Using ethnographic techniques, it analyses how this particular style of software development developed in a given locality, and how it uniquely hybridised documents, conversations, software tools and office layout in that locality. It examines some of the many artifices, devices, techniques and talk that come together as a complicated contemporary software system is produced. It argues that XP's emphasis on programming as the core activity and governing metaphor can only be understood in relation to competing overtly formal software engineering approaches and the organisational framing of software development. XP, it suggests, gains traction by re-embodying the habits of programming as a collective practice.
The TAB book of Arduino projects : 36 things to make with shields and protoshields
In this easy-to-follow book, electronics guru Simon Monk show you how to create a wide variety of fun and functional gadgets with the Arduino Uno and Leonardo boards. Filled with step-by-step instructions and detailed illustrations, The TAB Book of Arduino Projects: 36 Things to Make with Shields and Proto Shields provides a cost estimate, difficulty level, and list of required components for each project. You'll learn how to design custom circuits with Proto Shields and solder parts to the prototyping area to build professional-quality devices. Catapult your Arduino skills to the next level with this hands-on guide.
A Model for Schema Evolution in Object-Oriented Database Systems
The schema of a database is often considered to be static. However, in the life-time of a system, the schema is likely to be altered to accommodate changes in the requirements for data storage of the system. Such alterations may be the result of changes in the real world that the database is to model. For example, a database that is used to model the life of a chemical plant will need to evolve as the plant moves through the phases of design, commissioning, running and decommissioning. Each stage will have different data storage requirements. Changing the schema of a database has an impact on both the existing data and external agents that act on the database assuming a schema that may have been changed.Existing databases provide very little support for schema evolution. Object-oriented databases with their inherently flexible architectures are beginning to address this problem. The work described in this thesis is driven by the need to provide support for schema evolution in such a way that the data can retain its consistency with the schema and external agents acting on the database can continue to function after the schema of the database has been changed.A model for supporting schema evolution using multiple versions of class definitions has been developed and prototyped. This model provides better support for schema evolution than existing systems, that are based on class versioning, by using dynamic instance conversion rather than the instance emulation strategies employed in comparable systems. Graphical tools to support schema evolution have also been built to facilitate the process of changing a schema.As a secondary issue, the underlying mechanism developed to support schema evolution was also found to be applicable to the problem of providing views of classes; similar in concept to views in the relational database model.
Make : action : movement, light, and sound with Arduino and Raspberry Pi
Beginning with the basics and moving gradually to greater challenges, this book takes you step-by-step through experiments and projects that show you how to make your Arduino or Raspberry Pi create and control movement, light, and sound. In other words: action! The Arduino is a simple microcontroller with an easy-to-learn programming environment, while the Raspberry Pi is a tiny Linux-based computer. This book clearly explains the differences between the Arduino and Raspberry Pi, when to use them, and to which purposes each are best suited. Using these widely available and inexpensive platforms, you'll learn to control LEDs, motors of various types, solenoids, AC (alternating current) devices, heaters, coolers, displays, and sound. You'll even discover how to monitor and control these devices over the Internet. Working with solderless breadboards, you'll get up and running quickly, learning how to make projects that are as fun as they are informative. In Make:..
Revision indications for medial unicompartmental knee arthroplasty: a systematic review
IntroductionUnicompartmental knee arthroplasty (UKA) has advantages over total knee arthroplasty including fewer complications and faster recovery; however, UKAs also have higher revision rates. Understanding reasons for UKA failure may, therefore, allow for optimized clinical outcomes. We aimed to identify failure modes for medial UKAs, and to examine differences by implant bearing, cement use and time.Materials and methodsA systematic review was conducted by searching MedLine, EMBASE, CINAHL and Cochrane databases from 2000 to 2020. Studies were selected if they included ≥ 250 participants, ≥ 10 failures and reported all failure modes of medial UKA performed for osteoarthritis (OA).ResultsA total of 24 cohort and 2 registry-based studies (levels II and III) were selected. The most common failure modes were aseptic loosening (24%) and OA progression (30%). Earliest failures (< 6 months) were due to infection (40%), bearing dislocation (20%), and fracture (20%); mid-term failures (> 2 years to 5 years) were due to OA progression (33%), aseptic loosening (17%) and pain (21%); and late-term (> 10 years) failures were mostly due to OA progression (56%). Rates of failure from wear were higher with fixed-bearing prostheses (5% cf. 0.3%), whereas rates of bearing dislocations were higher with mobile-bearing prostheses (14% cf. 0%). With cemented components, there was a high rate of failure due to aseptic loosening (27%), which was reduced with uncemented components (4%).ConclusionsUKA failure modes differ depending on implant design, cement use and time from surgery. There should be careful consideration of implant options and patient selection for UKA.
Regulation of miRNA Transcription in Macrophages in Response to Candida albicans
Macrophages detect pathogens via pattern recognition receptors (PRRs), which trigger several intracellular signaling cascades including the MAPK and NFκB pathways. These in turn mediate the up-regulation of pro-inflammatory cytokines that are essential to combat the pathogen. However as the over-production of pro-inflammatory cytokines results in tissue damage or septic shock, precise control of these signaling pathways is essential and achieved via the induction of multiple negative feedback mechanisms. miRNAs are small regulatory RNAs that are able to affect protein expression, via the regulation of either mRNA stability or translation. Up-regulation of specific miRNAs could have the potential to modulate PRR signaling, as has been shown for both miR-146 and miR-155. Here we have analysed which miRNAs are up-regulated in mouse macrophages in response to the fungal pathogen heat killed Candida albicans and compared the profile to that obtained with the TLR4 ligand LPS. We found that in addition to miR-146 and miR-155, both Candida albicans and LPS were also able to up-regulate miR-455 and miR-125a. Analysis of the signaling pathways required showed that NFκB was necessary for the transcription of all 4 pri-miRNAs, while the ERK1/2 and p38 MAPK pathways were also required for pri-miR-125a transcription. In addition the anti-inflammatory cytokine IL-10 was found to be able to induce miR-146a and b, but inhibited miR-155 induction. These results suggest that miR-455, miR-125, miR-146 and miR-155 may play important roles in regulating macrophage function following PRR stimulation.
Hacking electronics : learning electronics with Arduino® and Raspberry Pi
Up-to-date hacks that will breathe life into your Arduino and Raspberry Pi creations! This intuitive DIY guide shows how to wire, disassemble, tweak, and re-purpose household devices and integrate them with your Raspberry Pi and Arduino inventions. Packed with full-color illustrations, photos, and diagrams, Hacking Electronics: Learning Electronics with Arduino and Raspberry Pi, Second Edition, features fun, easy-to-follow projects.You'll discover how to build an Internet-controlled hacked electric toy, ultrasonic rangefinder, remote-controlled robotic rover, audio amp, slot car brakes and headlights--even a smart card reader!
The kinases MSK1 and MSK2 act as negative regulators of Toll-like receptor signaling
Uncontrolled TLR signaling results in excessive inflammation. Arthur and colleagues show that the kinases MSK1 and MSK2 orchestrate a feedback loop involving interleukin 10 and the phosphatase DUSP1 to control TLR4 signaling. The kinases MSK1 and MSK2 are activated 'downstream' of the p38 and Erk1/2 mitogen-activated protein kinases. Here we found that MSK1 and MSK2 were needed to limit the production of proinflammatory cytokines in response to stimulation of primary macrophages with lipopolysaccharide. By inducing transcription of the mitogen-activated protein kinase phosphatase DUSP1 and the anti-inflammatory cytokine interleukin 10, MSK1 and MSK2 exerted many negative feedback mechanisms. Deficiency in MSK1 and MSK2 prevented the binding of phosphorylated transcription factors CREB and ATF1 to the promoters of the genes encoding interleukin 10 and DUSP1. Mice doubly deficient in MSK1 and MSK2 were hypersensitive to lipopolysaccharide-induced endotoxic shock and showed prolonged inflammation in a model of toxic contact eczema induced by phorbol 12-myristate 13-acetate. Our results establish MSK1 and MSK2 as key components of negative feedback mechanisms needed to limit Toll-like receptor–driven inflammation.