An Effect of Co–W Barrier Sublayer on the Functional Characteristics of Au–Ru Contact Coatings

Funding Information: Funding: This work was supported by the Ministry of Education and Science of the Russian Federation in the frame of the state assignment FSSN-2020-0003. Publisher Copyright: © 2022 by the authors. Licensee MDPI, Basel, Switzerland.The performance characteristics (microhardness, porosity, roughness, and transient resistance) of Au–Ru coatings with and without the Co–W alloy barrier sublayer electrodeposited on the surface of contact blades of commercially produced reed switches were investigated. It was found that the barrier sublayer reduces the average roughness of the coatings without significant change in their porosity. The Au–Ru coatings without sublayer exhibited a greater variation in the transient resistance during an increase in the pressing force. The service time of reed switches with the barrier sublayer increased in both testing modes: in low-power (50 mV, 5 µA, 50 Hz) by more than 4 × 106 switching cycles, and in mean-power (12 V, 0.25 A, 50 Hz) by more than 1.8 × 106 switching cycles.publishersversionpublishe

Switching Properties of the Contact Coatings Based on Refractory Metals Alloys

Switching the properties of the Ag contact groups of an electromagnetic relay with the electrodeposited Ni-W and Co-W alloy coatings was studied. It is shown that these coatings are able to stabilize the spread of contact resistance within the entire test interval and to increase the service life of Ag contact groups from 2.3 × 106 to 4.5 × 106 commutation cycles. According to our research, the service life of coated contact groups is mainly determined by a change in the surface morphology caused by the electrical erosive transfer of the contact materials and to a lesser extent by the formation of poorly conductive adsorbed hydrocarbon films

Electrochemical Deposition of Ni–W Crack-Free Coatings

The main features of electrochemical deposition of coatings based on Ni–W binary alloy in the pulse current mode using pyrophosphate electrolytes were studied. Two electrolytes with a pH of 8.7 and 9.5 were used. The deposition was carried out with the current density varying in the range of 0.01–0.1 A·cm−2, and the duty cycle (the relative pulse duration) was changed within the range 20–100%. The surface morphology and elemental and phase composition of the coatings were studied by scanning electron microscopy, energy-dispersive X-ray microanalysis and X-ray diffractometry. The experimental conditions allowing us to achieve the maximum Faradaic efficiency and W content in the coatings were determined. It was found that the pulse current mode enabled the fabrication of crack-free coatings with a thickness greater than 6 μm

GPIHBP1 stabilizes lipoprotein lipase and prevents its inhibition by angiopoietin-like 3 and angiopoietin-like 4

Glycosylphosphatidylinositol-anchored HDL-binding protein (GPIHBP1) binds both LPL and chylomicrons, suggesting that GPIHBP1 is a platform for LPL-dependent processing of triglyceride (TG)-rich lipoproteins. Here, we investigated whether GPIHBP1 affects LPL activity in the absence and presence of LPL inhibitors angiopoietin-like (ANGPTL)3 and ANGPTL4. Like heparin, GPIHBP1 stabilized but did not activate LPL. ANGPTL4 potently inhibited nonstabilized LPL as well as heparin-stabilized LPL but not GPIHBP1-stabilized LPL. Like ANGPTL4, ANGPTL3 inhibited nonstabilized LPL but not GPIHBP1-stabilized LPL. ANGPTL3 also inhibited heparin-stabilized LPL but with less potency than nonstabilized LPL. Consistent with these in vitro findings, fasting serum TGs of Angptl4−/−/Gpihbp1−/− mice were lower than those of Gpihbp1−/− mice and approached those of wild-type littermates. In contrast, serum TGs of Angptl3−/−/Gpihbp1−/− mice were only slightly lower than those of Gpihbp1−/− mice. Treating Gpihbp1−/− mice with ANGPTL4- or ANGPTL3-neutralizing antibodies recapitulated the double knockout phenotypes. These data suggest that GPIHBP1 functions as an LPL stabilizer. Moreover, therapeutic agents that prevent LPL inhibition by ANGPTL4 or, to a lesser extent, ANGPTL3, may benefit individuals with hyperlipidemia caused by gene mutations associated with decreased LPL stability