Design and Operation of Front-End Electronics for the HERA-B Muon Detector

We have implemented a cost-effective design for the readout electronics of both the anode wires and the cathode pads of large area proportional wire chambers for the HERA-B muon system based on the ASD-08 integrated circuit. To control and monitor the large number of readout channels, we have built a distributed control system based on Philips Semiconductors' I2C bus and microcontrollers. To date we have installed about 10800 channels of muon chambers and electronics. The average single channel noise occupancy is less than 10**-5, and the detectors have been operated with target interaction rates as high as 70 MHz

Elevated 18:0 lysophosphatidylcholine contributes to the development of pain in tissue injury

Tissue injuries, including burns, are major causes of death and morbidity worldwide. These injuries result in the release of intracellular molecules and subsequent inflammatory reactions, changing the tissues’ chemical milieu and leading to the development of persistent pain through activating pain-sensing primary sensory neurons. However, the majority of pain-inducing agents in injured tissues are unknown. Here, we report that, amongst other important metabolite changes, lysophosphatidylcholines (LPCs) including 18:0 LPC exhibit significant and consistent local burn injury-induced changes in concentration. 18:0 LPC induces immediate pain and the development of hypersensitivities to mechanical and heat stimuli through molecules including the transient receptor potential ion channel, vanilloid sub-family, member 1 and member 2 at least partly via increasing lateral pressure in the membrane. As levels of LPCs including 18:0 LPC increase in other tissue injuries, our data reveal a novel role for these lipids in injury-associated pain. These findings have high potential to improve patient care