The ATLAS semiconductor tracker end-cap module

The challenges for the tracking detector systems at the LHC are unprecedented in terms of the number of channels, the required readout speed and the expected radiation levels. The ATLAS Semiconductor Tracker (SCT) end-caps have a total of about 3 million electronics channels each reading out every 25 ns into its own on-chip 3:3 ms buffer. The highest anticipated dose after 10 years operation is 1:4 1014 cm2 in units of 1 MeV neutron equivalent (assuming the damage factors scale with the non-ionising energy loss). The forward tracker has 1976 double-sided modules, mostly of area �70 cm2, each having 2 768 strips read out by six ASICs per side. The requirement to achieve an average perpendicular radiation length of 1.5% X0, while coping with up to 7W dissipation per module (after irradiation), leads to stringent constraints on the thermal design. The additional requirement of 1500e equivalent noise charge (ENC) rising to only 1800e ENC after irradiation, provides stringent design constraints on both the high-density Cu/Polyimide flex read-out circuit and the ABCD3TA read-out ASICs. Finally, the accuracy of module assembly must not compromise the 16 mm ðrfÞ resolution perpendicular to the strip directions or 580 mm radial resolution coming from the 40 mrad front-back stereo angle. A total of 2210 modules were built to the tight tolerances and specifications required for the SCT. This was 234 more than the 1976 required and represents a yield of 93%. The component flow was at times tight, but the module production rate of 40–50 per week was maintained despite this. The distributed production was not found to be a major logistical problem and it allowed additional flexibility to take advantage of where the effort was available, including any spare capacity, for building the end-cap modules. The collaboration that produced the ATLAS SCT end-cap modules kept in close contact at all times so that the effects of shortages or stoppages at different sites could be rapidly resolved

From Perception to Activation: The Molecular-Genetic and Biochemical Landscape of Disease Resistance Signaling in Plants

More than 60 years ago, H.H. Flor proposed the “Gene-for-Gene” hypothesis, which described the genetic relationship between host plants and pathogens. In the decades that followed Flor's seminal work, our understanding of the plant-pathogen interaction has evolved into a sophisticated model, detailing the molecular genetic and biochemical processes that control host-range, disease resistance signaling and susceptibility. The interaction between plants and microbes is an intimate exchange of signals that has evolved for millennia, resulting in the modification and adaptation of pathogen virulence strategies and host recognition elements. In total, plants have evolved mechanisms to combat the ever-changing landscape of biotic interactions bombarding their environment, while in parallel, plant pathogens have co-evolved mechanisms to sense and adapt to these changes. On average, the typical plant is susceptible to attack by dozens of microbial pathogens, yet in most cases, remains resistant to many of these challenges. The sum of research in our field has revealed that these interactions are regulated by multiple layers of intimately linked signaling networks. As an evolved model of Flor's initial observations, the current paradigm in host-pathogen interactions is that pathogen effector molecules, in large part, drive the recognition, activation and subsequent physiological responses in plants that give rise to resistance and susceptibility. In this Chapter, we will discuss our current understanding of the association between plants and microbial pathogens, detailing the pressures placed on both host and microbe to either maintain disease resistance, or induce susceptibility and disease. From recognition to transcriptional reprogramming, we will review current data and literature that has advanced the classical model of the Gene-for-Gene hypothesis to our current understanding of basal and effector triggered immunity