Partial Discharge Wideband Full-Band High-Gain Resonant Cavity UHF Sensor Research.

To meet the real demand for broadband full-band high-gain antenna sensors in the process of partial discharge (PD) Ultra-High frequency (UHF) detection test and online monitoring of power equipment, this paper builds a resonant cavity monopole UHF antenna sensor based on Fabry-Perot resonant cavity antenna technology, conducts the sensor Voltage Standing Wave Ratio (VSWR) optimization study using curved flow technology, conducts the sensor gain optimization study using slot dual resonant structure, and, finally, tests the sensor performance using the built PD detection test platform. The resonant cavity monopole antenna exhibits outstanding VSWR performance in the frequency range of 0.37 GHz-3 GHz, according to simulation and test data: the average gain in the frequency range of 0.3 GHz-3 GHz is 4.92 dBi, and the highest gain at the primary resonant frequency of 1.0 GHz is 7.16 dBi, with good radiation performance over the whole frequency spectrum. The electromagnetic pulse signal sensed by the UHF sensor developed in this paper can demonstrate the energy spectrum distribution characteristics of PD radiation electromagnetic wave signal more comprehensively, laying a firm technical foundation for thoroughly understanding the electromagnetic wave radiation characteristics of various types of PD insulation defects of various power equipment and the selection of a specific direction for its supporting optimization.

PD Flexible Built-In High-Sensitivity Elliptical Monopole Antenna Sensor.

In view of the insufficient signal detection sensitivity of Gas Insulated Switchgear (GIS), partial discharge (PD), ultra-high frequency (UHF), and failure to conform with GIS surface structure when the existing rigid stereo structure UHF sensor is built in, this paper, using rectangular patch antenna equivalent technique, trapezoidal ground plane technique, and coplanar waveguide (CPW) feed line index asymptotic linearization technique, conducts research on a flexible built-in high-sensitivity elliptic monopole antenna. The flexible antenna, with a thickness of only 0.28 mm, can be kept at a voltage standing wave ratio (VSWR) of less than three in the 300 MHz to 3 GHz band under the curvature radius of 0, 100, 300, and 500 mm, and at less than two in the 650 MHz to 3 GHz band. Through the true 220 kV-GIS partial discharge experimental platform built to analyze the high frequency electromagnetic wave detection performance of the built-in flexible antenna, it is shown that the flexible built-in high-sensitivity elliptical monopole antenna designed in this paper can effectively detect the characteristic signals of high-frequency electromagnetic waves emitted by partial discharges with an average discharge amount below 10 pC.

Flexible Planar Monopole Built-in GIS PD Sensor Based on Meandering Technology.

To address the problem of low space utilization of existing rigid Ultra-High Frequency (UHF) sensors for partial discharge (PD) in Gas-Insulated Switchgears (GIS) and the problem of disrupting the electric field distribution inside the GIS. This paper draws on the idea of flexible wearable antennas and introduces planar monopole antennas commonly used in the communication field as GIS PD detection sensors and carried out research on flexible planar monopole sensing technology built into GIS PD. The VSWR of monopole antenna in the UHF low band is optimized by the meandering technique. The size of the designed flexible antenna is 142 mm × 195 mm × 0.28 mm. The simulation and physical test results show that the improved monopole antenna with meandering technology has a VSWR of ≤2 in the frequency bands 570 MHz-830 MHz, 1.38 GHz-1.8 GHz, and 2.2 GHz-2.76 GHz when the bending radius is 0 mm, 200 mm, and 400 mm, respectively. The VSWR in the frequency band 450 MHz-3 GHz is ≤5. A 220 kV GIS PD detection platform was built to test the performance of the designed antenna, and the results showed that the antenna could detect the PD signal after bending deformation with a high Signal Noise Ratio (SNR).

Anti-Tumor Necrosis Factor Therapy and Incidence of Parkinson Disease Among Patients With Inflammatory Bowel Disease.

Importance: Despite established genetic and pathophysiologic links between inflammatory bowel disease (IBD) and Parkinson disease (PD), clinical data supporting this association remain scarce. Although systemic inflammation is considered a potential biological mechanism shared between the 2 diseases, the role of reduced systemic inflammation through IBD-directed anti-tumor necrosis factor (anti-TNF) therapy in PD risk is largely unknown. Objective: To compare the incidence of PD among individuals with or without IBD and to assess whether PD risk among patients with IBD is altered by anti-TNF therapy. Design, Setting, and Participants: This is a retrospective cohort study analyzing information in the Truven Health MarketScan administrative claims database and the Medicare Supplemental Database between January 1, 2000, and March 31, 2016. Individuals were selected who had at least 2 claims for IBD diagnoses, at least 6 months of follow-up, and no prior diagnosis of PD on or before the IBD index date. Exposure to Anti-TNF therapy was measured from the anti-TNF index date to the last date of anti-TNF coverage or the end of enrollment or PD index date, whichever was earliest. Incidence rates per 1000 person-years were calculated, and crude and adjusted incidence rate ratios were estimated by Poisson regression models and presented with 95% CIs. Main Outcomes and Measures: Incidence of PD among patients with IBD with or without exposure to anti-TNF therapy. Results: In total, 144 018 individuals with IBD were matched on age, sex, and year of index date with 720 090 unaffected controls. Of them, 1796 individuals had at least 2 PD diagnoses and at least 1 filled PD-related prescription. The mean (SD) age of individuals with IBD was 51 (17) years, and 44% were men. The incidence of PD among patients with IBD was 28% higher than that among unaffected matched controls (adjusted incidence rate ratio, 1.28; 95% CI, 1.14-1.44; P < .001). A 78% reduction in the incidence rate of PD was detected among patients with IBD who were exposed to anti-TNF therapy compared with those who were not exposed (adjusted incidence rate ratio, 0.22; 95% CI, 0.05-0.88; P = .03). Conclusions and Relevance: A higher incidence of PD was observed among patients with IBD than among individuals without IBD. Early exposure to antiinflammatory anti-TNF therapy was associated with substantially reduced PD incidence. These findings support a role of systemic inflammation in the pathogenesis of both diseases. Further studies are required to determine whether anti-TNF treatment administered to high-risk individuals may mitigate PD risk.

Activated AMPK inhibits PPAR-{alpha} and PPAR-{gamma} transcriptional activity in hepatoma cells.

AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor-α (PPAR-α) are critical regulators of short-term and long-term fatty acid oxidation, respectively. We examined whether the activities of these molecules were coordinately regulated. H4IIEC3 cells were transfected with PPAR-α and PPAR-γ expression plasmids and a peroxisome-proliferator-response element (PPRE) luciferase reporter plasmid. The cells were treated with PPAR agonists (WY-14,643 and rosiglitazone), AMPK activators 5-aminoimidazole-4-carboxamide riboside (AICAR) and metformin, and the AMPK inhibitor compound C. Both AICAR and metformin decreased basal and WY-14,643-stimulated PPAR-α activity; compound C increased agonist-stimulated reporter activity and partially reversed the effect of the AMPK activators. Similar effects on PPAR-γ were seen, with both AICAR and metformin inhibiting PPRE reporter activity. Compound C increased basal PPAR-γ activity and rosiglitazone-stimulated activity. In contrast, retinoic acid receptor-α (RAR-α), another nuclear receptor that dimerizes with retinoid X receptor (RXR), was largely unaffected by the AMPK activators. Compound C modestly increased AM580 (an RAR agonist)-stimulated activity. The AMPK activators did not affect PPAR-α binding to DNA, and there was no consistent correlation between effects of the AMPK activators and inhibitor on PPAR and the nuclear localization of AMPK-α subunits. Expression of either a constitutively active or dominant negative AMPK-α inhibited basal and WY-14,643-stimulated PPAR-α activity and basal and rosiglitazone-stimulated PPAR-γ activity. We concluded that the AMPK activators AICAR and metformin inhibited transcriptional activities of PPAR-α and PPAR-γ, whereas inhibition of AMPK with compound C activated both PPARs. The effects of AMPK do not appear to be mediated through effects on RXR or on PPAR/RXR binding to DNA. These effects are independent of kinase activity and instead appear to rely on the activated conformation of AMPK. AMPK inhibition of PPAR-α and -γ may allow for short-term processes to increase energy generation before the cells devote resources to increasing their capacity for fatty acid oxidation.