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Jul 28, 2011 8:53 am

An introduction to Pixar’s Tractor 1.0


As we head into SIGGRAPH 2011 coverage in the coming month we thought it would be useful to introduce some new or new-ish software tools that many in the 3D community may not yet know about–especially those (perhaps?) on the Mac side of the equation.

Pixar is famous for its movies and its RenderMan software. Those in the know, have known for quite some time now that Pixar’s RenderMan is back on the Mac in a big way but the company continues to develop software (most of it for exclusive internal use) and some of it is for distribution.

One such piece of software is Pixar’s Tractor. Tractor 1.0 is Pixar’s totally new, next-generation, distributed processing rendering solution. In other words, it is a network-intensive application for distributing software rendering tasks.

What makes Tractor special is that it is specifically engineered for extreme scalability and performance, ideal for multi-core networks with upwards of tens of thousands of processors–perhaps a hundred thousand processors or more.

Tractor is designed to replace Pixar’s Alfred and Alfserver, which are network rendering tools which are still in production. Both will be phased out over a term ending in June of 2012.

Tractor 1.0 has three parts. The Tractor-Engine maintains the central job queue and dispatch of tasks. Tractor-Blade is a Python based execution server running on each remote node. Finally, Tractor-Dashboard is a customizable web browser user interface providing centralized control of the Tractor-Engine.

Tractor 1.0 is based on a streamlined architecture designed for rapid deployment. The licensing model is simplified compared to Pixar’s Alfred products. Performance-wise it can deliver over 500 tasks per second to the queuing engine.

Tractor is extendable to non-rendering applications, such as compositing or physics simulations. A single license of Tractor 1.0 comes with each single license (or seat) of RenderMan Studio. No licenses come with RenderMan Pro Server. With this initial release Tractor 1.0 is intended to appeal to mid-sized to large installations of RenderMan.

Both RenderMan Studio and RenderMan for Autodesk Maya have full support for Tractor 1.0. Tractor is of course a multi-threaded application coded in C++ and responds to HTTP transaction requests and maintains a database of spooled jobs as a shallow (flat) hiearchy of files on desk.

Tractor 1.0 today is planned for dispatching RenderMan Pro Server tasks, but because of its extensibility will support plugins in the future for integration with other CG applications.

Na + currents: Whole cell Na + currents have not been measured in cells surviving in the healed infarcted heart. Intracellular sodium activity in the infarct zone does not differ from the normal zone tissues [13] , yet the increase in Na i activity in border zone tissue suggests a depressed Na + –K + pump activity and/or increased Na + leak in myocytes from the feline healed infarct model. These latter changes could indirectly affect V̇ max of APs of these myocytes [12] .

Ca 2+ currents: Myocytes adjacent to the 8-week infarct in the rabbit heart show a significant decrease in peak I CaL density without a change in current–voltage relations, voltage-dependence or steady-state inactivation kinetics [14] . In the 2-month feline infarct model, myocytes from the area underlying or immediately adjacent to the infarct scar also have reduced I CaL amplitudes at most test voltages [29] . These values differ from those of controls and from those cells dispersed from the remote regions of the same infarcted heart. Reduced current density and accelerated current decay persist even when barium is used as the charge carrier, suggesting a decrease in the number of functional Ca 2+ channels at this time. Steady-state activation and recovery from inactivation remain unchanged [29] . The voltage at which Ca 2+ channels are half-maximally available (inactivation curve) is shifted by 10 mV in the hyperpolarizing direction in MI myocytes. Consequently, the availability of the Ca 2+ channels in the voltage range −40 to +20 mV is changed, resulting in smaller L type Ca 2+ inward window currents than controls. The altered I CaL kinetic changes may partially account for decrements in the infarct zone total I CaL density and could contribute to a reduction in voltage and duration of phase 2 of the APs of cells of the healed infarct.

I to : Action potential recordings of the subendocardial Purkinje fibers that survive 24–48 h after occlusion have a small degree of rapid phase 1 of repolarization when fibers are driven at slow rates. Pacing at fast rates causes little or no change in phase 1 of repolarization in normal Purkinje fibers, yet it has a dramatic effect on the time course of repolarization of subendocardial Purkinje myocytes surviving in the infarcted heart. In some cases, with an increase in drive rate, the rapid phase 1 of repolarization of APs in these fibers completely disappears (see Fig. 3.30 of [1] ). Whole cell voltage clamp experiments have confirmed that the density and kinetics of I to in these cells is reduced by 51% and that these changes are not due to alterations in steady-state availability of the channel. I to currents in Purkinje myocytes from the 48-h infarcted heart also show specific kinetic changes. Notably, the time course of current decay is accelerated while the time course of reactivation of I to is significantly delayed. This slowing of I to recovery implies that less outward repolarizing current is available for APs occurring at high pacing rates or during closely spaced voltage clamp steps [31] .

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