The ATLAS level-1 central trigger system
The central part of the ATLAS Level-1 trigger system consists of the central trigger processor (CTP), the local trigger processors (LTPs), the timing, trigger, and control (TTC) system, and the read-out driver busy (ROD/spl I.bar/BUSY) modules. The CTP combines information from calorimeter and muon trigger processors, as well as from other sources, and makes the final Level-1 accept decision (L1A) on the basis of lists of selection criteria, implemented as trigger menus. Timing and trigger signals are fanned out to about 40 LTPs, which inject them into the subdetector TTC partitions. The LTPs also support stand-alone running and can generate all necessary signals from memory. The TTC partitions fan out the timing and trigger signals to the subdetector front-end electronics. The ROD/spl I.bar/BUSY modules receive busy signals from the front-end electronics, and send them to the CTP (via an LTP) to throttle the generation of L1As. An overview of the ATLAS Level-1 central trigger system will be presented, with emphasis on the design and tests of the CTP modules.
The ATLAS Level-1 Central Trigger Processor (CTP)
The ATLAS Level-1 Central Trigger Processor (CTP) com- bines information from the Level-1 calorimeter and muon trig- ger processors, as well as from other sources such as calibration triggers, and makes the final Level-1 Accept deci- sion. The CTP synchronises the trigger inputs from different sources to the internal clock and aligns them with respect to the same bunch crossing. The algorithm used by the CTP to com- bine the different inputs allows events to be selected on the basis of trigger menus. The CTP provides trigger summary information to the data acquisition and to the Level-2 trigger system, and allows one to monitor various counters of bunch- by-bunch as well as accumulated information on the trigger inputs. The design of the CTP with its six different module types and two dedicated back-planes will be presented.
Immune dysfunction following infection with chicken anemia agent and infectious bursal disease virus. II. Alterations of in vitro lymphoproliferation and in vivo immune responses.
To determine the functional impact of alterations in lymphocyte concentrations and ratios following infection with chicken anemia agent (CAA) alone or in combination with infectious bursal disease virus (IBDV) on the immune system of young chickens, in vitro lymphoproliferation assays and in vivo responses to vaccination with several common viral agents were assessed at various time intervals post-inoculation (PI). Concanavalin A (Con A), phytohemagglutinin (PHA) and pokeweed mitogen (PWM) stimulation of splenic lymphocytes (SPL) collected from control birds could not be detected until 10-14 days PI. Infection with CAA was characterized by significantly higher PWM stimulation of SPL at 17 days PI and significantly lower PWM stimulation of peripheral blood lymphocytes (PBL) at 14 days PI, compared with uninfected controls. Concanavalin A and PWM stimulation of SPL was significantly increased in birds inoculated with IBDV alone. Lymphocytes harvested from birds inoculated simultaneously with CAA and IBDV had significantly lower responses. Effects on humoral and cell-mediated immunity following CAA and/or IBDV were determined by evaluating vaccination responses to Newcastle disease virus (NDV), fowl pox virus (FPV) and infectious laryngotracheitis virus (ILTV) during the acute phase of CAA infection (2 weeks PI). Vaccination of birds 2 weeks following CAA infection at 1 day of age resulted in decreased protection against NDV (85.7%) and ILTV (7.1%) challenge compared with protection rates in control birds (100% and 53.3% respectively). Infectious bursal disease virus infection was associated with decreased protection against NDV (60%) only. Concomitant infection at 1 day of age resulted in a greater reduction in NDV challenge protection (33.3%), slightly decreased FPV protection (87.5%), increased numbers of persistent FPV vaccination lesions and increased protection against ILTV challenge (71.4%). Vaccination of birds 2 weeks following CAA infection at 2 weeks of age resulted in slightly decreased NDV humoral antibody, development of persistent FPV vaccination lesions (17%) and increased immunity to ILTV challenge compared with control birds (83.3% vs. 66.7%). Chickens inoculated with IBDV alone displayed a more severe depression in NDV antibody titers and only a slight decrease in ILTV protection. Vaccination following concomitant infection at 2 weeks of age resulted in a higher percentage of FPV persistent vaccination lesions (39%) and greatly enhanced immunity to ILTV challenge (100%).