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In order to reduce the volume and the radiotoxicity of the nuclear waste coming from the operation of existing pressurized water reactors, accelerator-driven systems (ADSs) have been envisioned. The Lead-Cooled (Pb) European Facility for Industrial-Scale Transmutation (EFIT) (Pb-EFIT) plant is the first ADS design that has been going into a rather detailed engineering level. It is a lead-cooled, 385-MW(thermal) ADS prototype for minor actinide (MA) transmutation designed to achieve an optimal MA destruction rate of [approximately]42 kg/TW·h(thermal).The spallation target unit is located in the center of the diagrid where 800-MeV protons from the accelerator impinge on a free surface of lead exposed to vacuum.The core inlet temperature was set at 400°C to assure a sufficiently large safety margin to lead freezing, and the core outlet temperature was limited to 480°C to allow acceptable corrosion. The ferritic-martensitic 9% Cr steel T91 protected against corrosion with alumina FeCrAlY [GESA (Gepulste Elektronen Strahl Anlage) treatment].The primary circuit is designed for effective natural circulation, i.e., relatively low pressure losses, and the design offers good protection for a heat removal system in case of a blackout accident. The EFIT plant is designed to have a low likelihood and a low degree of core damage, to eliminate the need for off-site emergency responses in case of a severe accident, to use an extensively reliable passive safety system to fulfill the safety functions, and to eliminate the need of alternating-current safety-grade power (no safety-grade diesel generator). Three systems contribute to the decay heat removal (DHR) function of Pb-EFIT: the steam generators, the direct reactor cooling system, and the isolation condenser system.The EFIT plant exhibits four primary pumps; eight steam generator units, each rated at 52 MW, provide heat removal under normal operation. On the secondary side, the water steam ensures a thermal efficiency of [approximately]40% with the superheated vapor secondary circuit, taking into account the electricity required by pumps (from both the primary circuit and the secondary circuits) but without deducing the power required for the accelerator.An estimate of the Pb-EFIT plant cost has been performed based mainly on experience and engineering judgment. A best estimate (base cost and contingency) of about €1890 million, with an overall uncertainty of 22%, has been found.

We have tested the hypothesis that α-adrenergic drive is involved in the nocturnal increase in TSH in man. Seven mildly hypothyroid women (basal TSH levels 5·0–11·0 mU/1), aged 38–60 years, and nine euthyroid women, aged 27–60 years, were studied. Subjects underwent α-adrenergic blockade by infusion of thymoxamine (210 μg/min from 19.00 to 24.00 h); the same women were used as controls, with saline infused on different nights. Subjects were not allowed to sleep during the study period.A clear evening rise in basal TSH levels was apparent in both normal subjects and patients. Although overall secretion of TSH was slightly decreased in normal subjects (mean ± s.e.m.area under the curve, 29·93 ± 0·96 vs 30·71 ±mU/1 per h; P<0·05), thymoxamine infusion did not produce any major alteration in the gradual rise in TSH levels during the evening (incremental change above baseline +0·96± 0·21 during control infusion and + 0·97 ± 0·27 mU/1 during thymoxamine infusion). In mildly hypothyroid patients the TSH changes were exaggerated and α-adrenergic blockade caused a reduction in basal TSH levels and a delayed rise in TSH (incremental change above baseline +2·93 ± 1·42 during control infusion and +2·26 ± 0·73 mU/1 during thymoxamine infusion; P< 0·02). Overall TSH secretion was significantly decreased by thymoxamine (mean ± s.e.m.area 106 ± 2·45 mU/1 per h vs 123·32 ± 3·68 in the control study; P<0·0001). As expected, no circadian change was observed in basal prolactin levels in either controls or patients.Although α-adrenergic pathways may play a role in modulating the nocturnal increase in basal TSH levels, our data suggest that the evening rise in TSH is not a consequence of a primary increase in α-adrenergic drive. The increased TSH changes of mildly hypothyroid patients may, however, be sustained by increased central α-adrenergic stimulation of the TSH secretion.J. Endocr.(1987) 115,187–191