Parametric amplification via superconducting contacts in a Ka band niobium pillbox cavity

Superconducting parametric amplifiers are commonly fabricated using planar transmission lines with a non-linear inductance provided by either Josephson junctions or the intrinsic kinetic inductance of the thin film. However, Banys et al. [1] reported non-linear behaviour in a niobium pillbox cavity, hypothesising that below Tc, the pair iris-bulk resonator would act as a superconducting contact surface exploiting a Josephson-like non-linearity. This work investigates this effect further by applying Keysight Technologies' Advanced Design System (ADS) to simulate the cavity using an equivalent circuit model that includes a user defined Josephson inductance component. The simulations show that for a resonance centred at nu0 = 30.649 GHz, when two tones (pump and signal) are injected into the cavity, mixing and parametric gain occur. The maximum achievable gain is explored when the resonator is taken to its bifurcation energy. These results are compared to cryogenic measurements where the pump and signal are provided by a Vector Network Analyzer

Measuring the Kapitza Resistance between a Passivated Semiconductor and Liquid Helium

In this paper, we describe an experimental investigation into the effect of passivation layer thickness on heat dissipation between a quartz substrate and liquid helium. We have observed that by depositing SiN from 0 to 240 nm, the Kapitza resistance increases by 0.0365 m^2.K/W per nanometer more than for an unpassivated semiconductor. We hypothesize that this increase in Kapitza resistance represents an additional barrier to the cooling of semiconductor devices in liquid helium.Comment: 7 page

The Impact of Surface Passivation on Kapitza Resistance at the Interface between a Semiconductor and Liquid Nitrogen

Cooling electronic devices to cryogenic temperatures (< 77 K) is crucial in various scientific and engineering domains. Efficient cooling involves the removal of heat generated from these devices through thermal contact with either a liquid cryogen or a dry cryostat cold stage. However, as these devices cool, thermal boundary resistance, also known as Kapitza resistance, hinders the heat flow across thermal interfaces, resulting in elevated device temperatures. In transistors, the presence of passivation layers like Silicon Nitride (SiN) introduces additional interfaces that further impede heat dissipation. This paper investigates the impact of passivation layer thickness on Kapitza resistance at the interface between a solid device and liquid nitrogen. The Kapitza resistance is measured using a capacitance thermometer that has been passivated with SiN layers ranging from 0 to 240 nm. We observe that Kapitza resistance increases with increasing passivation thickness.Comment: 6 pages, 5 Figure

Parametric amplification via superconducting contacts in a Ka band niobium pillbox cavity

Superconducting parametric amplifiers are commonly fabricated using planar transmission lines with a non-linear inductance provided by either Josephson junctions or the intrinsic kinetic inductance of the thin film. However, Banys et al. [1] reported non-linear behaviour in a niobium pillbox cavity, hypothesising that below Tc, the pair iris-bulk resonator would act as a superconducting contact surface exploiting a Josephson-like non-linearity. This work investigates this effect further by applying Keysight Technologies' Advanced Design System (ADS) to simulate the cavity using an equivalent circuit model that includes a user defined Josephson inductance component. The simulations show that for a resonance centred at nu0 = 30.649 GHz, when two tones (pump and signal) are injected into the cavity, mixing and parametric gain occur. The maximum achievable gain is explored when the resonator is taken to its bifurcation energy. These results are compared to cryogenic measurements where the pump and signal are provided by a Vector Network Analyzer

Remote conditioning or erythropoietin before surgery primes kidneys to clear ischemia-reperfusion-damaged cells: a renoprotective mechanism?

Acute kidney injury is common, serious with no specific treatment. Ischemia-reperfusion is a common cause of acute kidney injury (AKI). Clinical trials suggest that preoperative erythropoietin (EPO) or remote ischemic preconditioning may have a renoprotective effect. Using a porcine model of warm ischemia-reperfusion-induced AKI (40-min bilateral cross-clamping of renal arteries, 48-h reperfusion), we examined the renoprotective efficacy of EPO (1,000 iu/kg iv.) or remote ischemic preconditioning (3 cycles, 5-min inflation/deflation to 200 mmHg of a hindlimb sphygmomanometer cuff). Ischemia-reperfusion induced significant kidney injury at 24 and 48 h (χ(2), 1 degree of freedom, >10 for 6/7 histopathological features). At 2 h, a panel of biomarkers including plasma creatinine, neutrophil gelatinase-associated lipocalin, and IL-1β, and urinary albumin:creatinine could be used to predict histopathological injury. Ischemia-reperfusion increased cell proliferation and apoptosis in the renal cortex but, for pretreated groups, the apoptotic cells were predominantly intratubular rather than interstitial. At 48-h reperfusion, plasma IL-1β and the number of subcapsular cells in G2-M arrest were reduced after preoperative EPO, but not after remote ischemic preconditioning. These data suggest an intrarenal mechanism acting within cortical cells that may underpin a renoprotective function for preoperative EPO and, to a limited extent, remote ischemic preconditioning. Despite equivocal longer-term outcomes in clinical studies investigating EPO as a renoprotective agent in AKI, optimal clinical dosing and administration have not been established. Our data suggest further clinical studies on the potential renoprotective effect of EPO and remote ischemic preconditioning are justified

Simple, Defensible Sample Sizes Based on Cost Efficiency -- With Discussion and Rejoinder

The conventional approach of choosing sample size to provide 80% or greater power ignores the cost implications of different sample size choices. Costs, however, are often impossible for investigators and funders to ignore in actual practice. Here, we propose and justify a new approach for choosing sample size based on cost efficiency, the ratio of a study’s projected scientific and/or practical value to its total cost. By showing that a study’s projected value exhibits diminishing marginal returns as a function of increasing sample size for a wide variety of definitions of study value, we are able to develop two simple choices that can be defended as more cost efficient than any larger sample size. The first is to choose the sample size that minimizes the average cost per subject. The second is to choose sample size to minimize total cost divided by the square root of sample size. This latter method is theoretically more justifiable for innovative studies, but also performs reasonably well and has some justification in other cases. For example, if projected study value is assumed to be proportional to power at a specific alternative and total cost is a linear function of sample size, then this approach is guaranteed either to produce more than 90% power or to be more cost efficient than any sample size that does. These methods are easy to implement, based on reliable inputs, and well justified, so they should be regarded as acceptable alternatives to current conventional approaches

Oligodendroglial modulation of fast axonal transport in a mouse model of hereditary spastic paraplegia

Oligodendrocytes are critical for the development of the plasma membrane and cytoskeleton of the axon. In this paper, we show that fast axonal transport is also dependent on the oligodendrocyte. Using a mouse model of hereditary spastic paraplegia type 2 due to a null mutation of the myelin Plp gene, we find a progressive impairment in fast retrograde and anterograde transport. Increased levels of retrograde motor protein subunits are associated with accumulation of membranous organelles distal to nodal complexes. Using cell transplantation, we show categorically that the axonal phenotype is related to the presence of the overlying Plp null myelin. Our data demonstrate a novel role for oligodendrocytes in the local regulation of axonal function and have implications for the axonal loss associated with secondary progressive multiple sclerosis

What does my patient's coronary artery calcium score mean? Combining information from the coronary artery calcium score with information from conventional risk factors to estimate coronary heart disease risk

Abstract: Background: The coronary artery calcium (CAC) score is an independent predictor of coronary heart disease. We sought to combine information from the CAC score with information from conventional cardiac risk factors to produce post-test risk estimates, and to determine whether the score may add clinically useful information. Methods: We measured the independent cross-sectional associations between conventional cardiac risk factors and the CAC score among asymptomatic persons referred for non-contrast electron beam computed tomography. Using the resulting multivariable models and published CAC score-specific relative risk estimates, we estimated post-test coronary heart disease risk in a number of different scenarios. Results: Among 9341 asymptomatic study participants (age 35-88 years, 40% female), we found that conventional coronary heart disease risk factors including age, male sex, self-reported hypertension, diabetes and high cholesterol were independent predictors of the CAC score, and we used the resulting multivariable models for predicting post-test risk in a variety of scenarios. Our models predicted, for example, that a 60-year-old non-smoking non-diabetic women with hypertension and high cholesterol would have a 47% chance of having a CAC score of zero, reducing her 10-year risk estimate from 15% (per Framingham) to 6-9%; if her score were over 100, however (a 17% chance), her risk estimate would be markedly higher (25-51% in 10 years). In low risk scenarios, the CAC score is very likely to be zero or low, and unlikely to change management. Conclusion: Combining information from the CAC score with information from conventional risk factors can change assessment of coronary heart disease risk to an extent that may be clinically important, especially when the pre-test 10-year risk estimate is intermediate. The attached spreadsheet makes these calculations easy