ITER LHe Plants Parallel Operation

AbstractThe ITER Cryogenic System includes three identical liquid helium (LHe) plants, with a total average cooling capacity equivalent to 75kW at 4.5K.The LHe plants provide the 4.5 K cooling power to the magnets and cryopumps. They are designed to operate in parallel and to handle heavy load variations.In this proceedingwe will describe the presentstatusof the ITER LHe plants with emphasis on i) the project schedule, ii) the plantscharacteristics/layout and iii) the basic principles and control strategies for a stable operation of the three LHe plants in parallel

Nonlinear control of a membrane mirror strip actuated axially and in bending

The sliding mode technique is used to control the deformation of a membrane mirror strip augmented with two macrofiber composite bimorphs located near the ends of the strip. The first bimorph is actuated in bending and the second is actuated axially. The structure is modeled as an Euler–Bernoulli beam under tensile load and the macrofiber composite patches are modeled as monolithic piezoceramic wafers. To cast the system into a finitedimensional state-space form, the finite element method is used, and the model presented accounts for the dynamics of the augmented bimorphs. The membrane strip is placed under uniform tension. Because one of the bimorphs acts axially, the resulting tension in the membrane strip is discontinuous at the location of this bimorph and, consequently, the obtained model is nonlinear. First, we validate the model experimentally by considering the system in its quasilinear state, then we consider the control problem. We formulate the regulation problem by using the sliding mode technique. Additionally, to allow coupling this system with an adaptive optics scheme, the shape-control problem is considered as well. The control law uses both actuators: the bending and axial bimorphs. However, a system singularity dictates using a switching command to avoid this singularity. Various examples are presented for the regulation and shape-control problems. The simulation results demonstrate the efficacy of the proposed control law

Effects of combined neutral endopeptidase 24-11 and angiotensin-converting enzyme inhibition on femoral vascular conductance in streptozotocin-induced diabetic rats

1. The successive effects of the angiotensin-converting enzyme inhibitor captopril (CAP, 2 mg kg(−1)+1 mg kg(−1) 30 min(−1) infusion) and the neutral endopeptidase 24-11 inhibitor retrothiorphan (RT, 25 mg kg(−1)+12.5 mg kg(−1) 30 min(−1) infusion) were studied on femoral vascular conductance (FVC) in streptozotocin-induced diabetic (STZ-SD) and control Sprague-Dawley (C-SD) rats. The role of the kinin-nitric oxide (NO) pathway was assessed by (1) using pre-treatments: a bradykinin (BK) B2 receptor antagonist (Hoe-140, 300 μg kg(−1)), a NO-synthase inhibitor (N(ω)-nitro-L-arginine methyl ester, L-NAME, 10 mg kg(−1)), a kininase I inhibitor (DL-2-mercaptomethyl-3-guanidinoethylthiopropanoic acid, MGTA, 10 mg kg(−1)+20 mg kg(−1) 20 min(−1) infusion) and (2) comparing the effects in STZ-induced diabetic (STZ-BN) and control Brown-Norway kininogen-deficient (C-BN) rats. 2. In C-SDs, CAP and CAP+RT increased FVC similarly. In STZ-SDs, FVC and FBF were decreased compared to C-SDs. CAP+RT increased them more effectively than CAP alone. 3. In both C-SDs and STZ-SDs, the femoral bed vasodilatation elicited by CAP was inhibited by Hoe-140 and L-NAME. The FVC increase elicited by CAP+RT was not significantly reduced by Hoe-140 but was inhibited by L-NAME and Hoe-140+MGTA. 4. In C-BNs, the vasodilatator responses to CAP and CAP+RT were abolished and highly reduced, respectively. In STZ-BNs, these responses were abolished. 5. These results show that in STZ-SDs, CAP+RT improve FBF and FVC more effectively than CAP alone. These effects are linked to an increased activation of the kinin-NO pathway. BK could lead to NO production by BK B2 receptor activation and another pathway in which kininase I may be involved

Melioidosis.

Burkholderia pseudomallei is a Gram-negative environmental bacterium and the aetiological agent of melioidosis, a life-threatening infection that is estimated to account for ∼89,000 deaths per year worldwide. Diabetes mellitus is a major risk factor for melioidosis, and the global diabetes pandemic could increase the number of fatalities caused by melioidosis. Melioidosis is endemic across tropical areas, especially in southeast Asia and northern Australia. Disease manifestations can range from acute septicaemia to chronic infection, as the facultative intracellular lifestyle and virulence factors of B. pseudomallei promote survival and persistence of the pathogen within a broad range of cells, and the bacteria can manipulate the host's immune responses and signalling pathways to escape surveillance. The majority of patients present with sepsis, but specific clinical presentations and their severity vary depending on the route of bacterial entry (skin penetration, inhalation or ingestion), host immune function and bacterial strain and load. Diagnosis is based on clinical and epidemiological features as well as bacterial culture. Treatment requires long-term intravenous and oral antibiotic courses. Delays in treatment due to difficulties in clinical recognition and laboratory diagnosis often lead to poor outcomes and mortality can exceed 40% in some regions. Research into B. pseudomallei is increasing, owing to the biothreat potential of this pathogen and increasing awareness of the disease and its burden; however, better diagnostic tests are needed to improve early confirmation of diagnosis, which would enable better therapeutic efficacy and survival