13 research outputs found

    Commissioning of the cryogenic safety test facility PICARD

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    The sizing of cryogenic safety relief devices requires detailed knowledge on the evolution of the pressure increase in cryostats following hazardous incidents such as the venting of the insulating vacuum with atmospheric air. Based on typical design and operating conditions in liquid helium cryostats, the new test facility PICARD, which stands for Pressure Increase in Cryostats and Analysis of Relief Devices, has been constructed. The vacuum-insulated test stand has a cryogenic liquid volume of 100 liters and a nominal design pressure of 16 bar(g). This allows a broad range of experimental conditions with cryogenic fluids. In case of helium, mass flow rates through safety valves and rupture disks up to about 4 kg/s can be measured. Beside flow rate measurements under various conditions (venting diameter, insulation, working fluid, liquid level, set pressure), the test stand will be used for studies on the impact of two-phase flow and for the measurement of flow coeffcients of safety devices at low temperature. This paper describes the operating range, layout and instrumentation of the test stand and presents the status of the commissioning phase

    Signal-to-noise ratio of temperature measurement with Cernox sensors at various supply currents

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    The Karlsruhe Institute of Technology (KIT) has developed a new thermal method for flow measurement, which is particularly suitable for the application in cryogenic systems. In this method, the stability and the resolution of temperature measurement is important, rather than precision. In other words, constant offsets in temperature measurements can be ignored, and the temperature sensors can be operated at supply currents beyond their nominal design value in order to gain resolution. For this application, the performance of two Cernox TM type CX-1050-SD-HT-1.4L sensors was measured in a temperature range between 300 K and 4 K. The experiments were carried out in the calibration cryostat at the Institute for Technical Physics. Sensors were connected to a Lake Shore Model 121 current source and a Keithley 2701/E digital multimeter for voltage measurements. At constant calibration temperatures, the supply currents were varied such that the resulting voltage drops lay in-between 10 mV and 100 mV. The influence on both the noise and the temperature offset are presented

    Intranight polarization variability in radio-loud and radio-quiet AGN

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    (Abriged) Intranight polarization variability in AGN has not been studied extensively so far. Studying the variability in polarization makes it possibly to distinguish between different emission mechanisms. Thus it can help answering the question if intranight variability in radio-loud and radio-quiet AGN is of the same or of fundamentally different origin. In this paper we investigate intranight polarization variability in AGN. Our sample consists of 28 AGN at low to moderate redshifts (0.048 < z < 1.036), 12 of which are radio-quiet quasars (RQQs) and 16 are radio-loud blazars. The subsample of blazars consists of eight flat-spectrum radio-quasars (FSRQs) and eight BL Lac objects. We find clear differences between the two samples. A majority of the radio-loud AGN show moderate to high degrees of polarization, more than half of them also show variability in polarization. There seems to be a dividing line for polarization intranight variability at P~5 per cent over which all objects vary in polarization. Only two out of 12 radio-quiet quasars show polarized emission, both at levels of P<1 per cent. The lack of polarization intranight variability in radio-quiet AGN points towards accretion instabilities being the cause for intranight flux variability whereas the high duty cycle of polarization variability in radio-loud objects is more likely caused by instabilities in the jet or changes of physical conditions in the jet plasma.Comment: Accepted for Publication in MNRAS (17 pages, 14 figures, 4 tables

    First experimental data of the cryogenic safety test facility PICARD

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    The test facility PICARD, which stands for Pressure Increase in Cryostats and Analysis of Relief Devices, has been designed and constructed for cryogenic safety experiments. With a cryogenic liquid volume of 100 L, a nominal design pressure of 16 bar(g) and the capacity of measuring helium mass flow rates through safety relief devices up to 4 kg/s, the test facility allows the systematic investigation of hazardous incidents in cryostats under realistic conditions. In the course of experiments, the insulating vacuum is vented with atmospheric air or gaseous nitrogen at ambient temperature under variation of the venting diameter, the thermal insulation, the cryogenic fluid, the liquid level and the set pressure in order to analyze the impact on the heat flux and hence on the process dynamics. A special focus will be on the occurrence and implications of two-phase flow during expansion and on measuring the flow coefficients of safety devices at cryogenic temperatures. This paper describes the commissioning and the general performance of the test facility at liquid helium temperatures. Furthermore, the results of first venting experiments are presented

    P2Y12 Inhibition in Murine Myocarditis Results in Reduced Platelet Infiltration and Preserved Ejection Fraction

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    Previous mouse studies have shown the increased presence of platelets in the myocardium during early stages of myocarditis and their selective detection by MRI. Here, we aimed to depict early myocarditis using molecular contrast-enhanced ultrasound of activated platelets, and to evaluate the impact of a P2Y12 receptor platelet inhibition. Experimental autoimmune myocarditis was induced in BALB/c mice by subcutaneous injection of porcine cardiac myosin and complete Freund adjuvant (CFA). Activated platelets were targeted with microbubbles (MB) coupled to a single-chain antibody that binds to the “ligand-induced binding sites” of the GPIIb/IIIa-receptor (=LIBS-MB). Alongside myocarditis induction, a group of mice received a daily dose of 100 g prasugrel for 1 month. Mice injected with myosin and CFA had a significantly deteriorated ejection fraction and histological inflammation on day 28 compared to mice only injected with myosin. Platelets infiltrated the myocardium before reduction in ejection fraction could be detected by echocardiography. No selective binding of the LIBS-MB contrast agent could be detected by either ultrasound or histology. Prasugrel therapy preserved ejection fraction and significantly reduced platelet aggregates in the myocardium compared to mice without prasugrel therapy. Therefore, P2Y12 inhibition could be a promising early therapeutic target in myocarditis, requiring further investigation

    Myeloid cell-specific Irf5 deficiency stabilizes atherosclerotic plaques in Apoe–/– mice

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    Objective: Interferon regulatory factor (IRF) 5 is a transcription factor known for promoting M1 type macrophage polarization in vitro. Given the central role of inflammatory macrophages in promoting atherosclerotic plaque progression, we hypothesize that myeloid cell-specific deletion of IRF5 is protective against atherosclerosis. Methods: Female Apoe–/– LysmCre/+ Irf5fl/fl and Apoe −/− Irf5fl/fl mice were fed a high-cholesterol diet for three months. Atherosclerotic plaque size and compositions as well as inflammatory gene expression were analyzed. Mechanistically, IRF5-dependent bone marrow-derived macrophage cytokine profiles were tested under M1 and M2 polarizing conditions. Mixed bone marrow chimeras were generated to determine intrinsic IRF5-dependent effects on macrophage accumulation in atherosclerotic plaques. Results: Myeloid cell-specific Irf5 deficiency blunted LPS/IFNγ-induced inflammatory gene expression in vitro and in the atherosclerotic aorta in vivo. While atherosclerotic lesion size was not reduced in myeloid cell-specific Irf5-deficient Apoe–/– mice, plaque composition was favorably altered, resembling a stable plaque phenotype with reduced macrophage and lipid contents, reduced inflammatory gene expression and increased collagen deposition alongside elevated Mertk and Tgfβ expression. Irf5-deficient macrophages, when directly competing with wild type macrophages in the same mouse, were less prone to accumulate in atherosclerotic lesion, independent of monocyte recruitment. Irf5-deficient monocytes, when exposed to oxidized low density lipoprotein, were less likely to differentiate into macrophage foam cells, and Irf5-deficient macrophages proliferated less in the plaque. Conclusion: Our study provides genetic evidence that selectively altering macrophage polarization induces a stable plaque phenotype in mice
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