A Closed-Form Expression for Estimating Radiated Emissions from the Power Planes in a Populated Printed Circuit Board

An expression for the maximum intensity of radiated emissions from a rectangular power bus structure has been derived based on an analytical cavity-resonator model. The effect of components mounted on the board is modeled by modifying the propagation constant of the waves within the power bus structure. The radiated field intensity is calculated using the equivalent magnetic current around the edges of the power bus structure together with the modified propagation constant. Measurements of a populated test board show that the derived closed-form expression estimates the level of the maximum radiation intensity with reasonable accuracy

20-H Rule Modeling and Measurements

The 20-H rule is a printed circuit board layout guideline. On boards with power and ground planes, the fringing field at the edges of the board is contained by backing the edge of the power plane away from the edge of the board by a distance equal to 20 times the separation distance between the planes. In this study, test boards were built and measured with and without implementing the 20-H rule. The measured results are compared to numerical models. The results of this study show that, although the near fields are more contained, the radiation from a board implementing the 20-H rule is actually slightly higher than the radiation from boards with a traditional desig

Derivation of a Closed-Form Approximate Expression for the Self-Capacitance of a Printed Circuit Board Trace

The electric fields that couple traces on printed circuit boards to attached cables can generate common-mode currents that result in significant radiated emissions. Previous work has shown that these radiated emissions can be estimated based on the self-capacitances of the microstrip structures on a board . In general, the determination of these self-capacitances must be done numerically using three-dimensional static modeling software. In this paper, an approximate closed-form expression for the self-capacitance of microstrip traces is derived. This expression can be used to estimate the voltage-driven common-mode emissions from boards with various microstrip trace geometries. The expression also provides insight relative to the microstrip parameters that have the greatest effect on radiated emissions

Model for Estimating Radiated Emissions from a Printed Circuit Board with Attached Cables Due to Voltage-Driven Sources

Common-mode currents induced on cables attached to printed circuit boards (PCBs) can be a significant source of unintentional radiated emissions. This paper develops a model for estimating the amount of common-mode cable current that can be induced by the signal voltage on microstrip trace structures or heatsinks on a PCB. The model employs static electric field solvers or closed-form expressions to estimate the effective self-capacitances of the board, trace, and/or heatsink. These capacitances are then used to determine the amplitude of an equivalent common-mode voltage source that drives the attached cables. The model shows that these voltage-driven common-mode cable currents are relatively independent of the cable parameters and the trace or heatsink location when the PCB is small relative to the cable length and to a wavelength

Drug-induced cough

© 2020, Czech Academy of Sciences. Since the recognition of angiotensin-converting enzyme inhibitors (ACEIs)-induced cough, drug has been considered as a potential cause of chronic cough. This review presents recent knowledge on drug-induced coughs in patients with chronic cough. The focus is placed on ACEIs, for which there are a multitude of studies documenting their associations with cough. Additional drugs are discussed for which there are reports of cough as a side effect of treatment, and the potential mechanisms of these effects are discussed

Decoupling Strategies for Printed Circuit Boards Without Power Planes

Traditional decoupling capacitors connected between V/CC/ and GND traces can be relatively ineffective at frequencies above their self-resonant frequency. This paper evaluates decoupling capacitor mounting strategies on boards without power planes. Techniques for minimizing mutual inductance and improving decoupling at frequencies above resonance are investigated

Expert System Algorithms for Identifying Radiated Emission Problems in Printed Circuit Boards

Radiated emission algorithms for a printed circuit board EMC expert system are described. The expert system mimics the thinking processes that human EMC engineers would use to analyze circuit boards and make design recommendations. Working with limited information about the enclosure, cables or the exact nature of the signals, the expert system evaluates different structures on the printed circuit board looking for potentially strong radiated emission sources. Results obtained from the analysis of a sample printed circuit board are provided to demonstrate how the expert system quickly identifies problems that would otherwise be difficult to locate

TRPV1-expressing primary afferents generate behavioral responses to pruritogens via multiple mechanisms

The mechanisms that generate itch are poorly understood at both the molecular and cellular levels despite its clinical importance. To explore the peripheral neuronal mechanisms underlying itch, we assessed the behavioral responses (scratching) produced by s.c. injection of various pruritogens in PLCβ3- or TRPV1-deficient mice. We provide evidence that at least 3 different molecular pathways contribute to the transduction of itch responses to different pruritogens: 1) histamine requires the function of both PLCβ3 and the TRPV1 channel; 2) serotonin, or a selective agonist, α-methyl-serotonin (α-Me-5-HT), requires the presence of PLCβ3 but not TRPV1, and 3) endothelin-1 (ET-1) does not require either PLCβ3 or TRPV1. To determine whether the activity of these molecules is represented in a particular subpopulation of sensory neurons, we examined the behavioral consequences of selectively eliminating 2 nonoverlapping subsets of nociceptors. The genetic ablation of MrgprD^+ neurons that represent ≈90% of cutaneous nonpeptidergic neurons did not affect the scratching responses to a number of pruritogens. In contrast, chemical ablation of the central branch of TRPV1+ nociceptors led to a significant behavioral deficit for pruritogens, including α-Me-5-HT and ET-1, that is, the TRPV1-expressing nociceptor was required, whether or not TRPV1 itself was essential. Thus, TRPV1 neurons are equipped with multiple signaling mechanisms that respond to different pruritogens. Some of these require TRPV1 function; others use alternate signal transduction pathways

Xylitol production is increased by expression of codon-optimized Neurospora crassa xylose reductase gene in Candida tropicalis

Xylose reductase (XR) is the first enzyme in d-xylose metabolism, catalyzing the reduction of d-xylose to xylitol. Formation of XR in the yeast Candida tropicalis is significantly repressed in cells grown on medium that contains glucose as carbon and energy source, because of the repressive effect of glucose. This is one reason why glucose is not a suitable co-substrate for cell growth in industrial xylitol production. XR from the ascomycete Neurospora crassa (NcXR) has high catalytic efficiency; however, NcXR is not expressed in C. tropicalis because of difference in codon usage between the two species. In this study, NcXR codons were changed to those preferred in C. tropicalis. This codon-optimized NcXR gene (termed NXRG) was placed under control of a constitutive glyceraldehyde-3-phosphate dehydrogenase (GAPDH) promoter derived from C. tropicalis, and integrated into the genome of xylitol dehydrogenase gene (XYL2)-disrupted C. tropicalis. High expression level of NXRG was confirmed by determining XR activity in cells grown on glucose medium. The resulting recombinant strain, LNG2, showed high XR activity (2.86 U (mg of protein)−1), whereas parent strain BSXDH-3 showed no activity. In xylitol fermentation using glucose as a co-substrate with xylose, LNG2 showed xylitol production rate 1.44 g L−1 h−1 and xylitol yield of 96% at 44 h, which were 73 and 62%, respectively, higher than corresponding values for BSXDH-3 (rate 0.83 g L−1 h−1; yield 59%)

CSF total tau/α-synuclein ratio improved the diagnostic performance for Alzheimers disease as an indicator of tau phosphorylation

Abstract Background Recently, several studies suggested potential involvements of α-synuclein in Alzheimers disease (AD) pathophysiology. Higher concentrations of α-synuclein were reported in cerebrospinal fluid (CSF) of AD patients with a positive correlation towards CSF tau, indicating its possible role in AD. We analyzed the CSF biomarkers to verify whether α-synuclein could be an additional supported biomarker in AD diagnosis. Methods In this cross-sectional study, CSF samples of 71 early-onset AD, 34 late-onset AD, 11 mild cognitive impairment, 17 subjective cognitive decline, 45 Parkinsons disease, and 32 healthy control (HC) were collected. CSF amyloid-β1-42 (A), total tau (N), and phosphorylated tau181 (T) were measured by commercial ELISA kits, and in-house ELISA kit was developed to quantify α-synuclein. The cognitive assessments and amyloid-PET imaging were also performed. Results CSF α-synuclein manifested a tendency to increase in AD and to decreased in Parkinsons disease compared to HC. The equilibrium states of total tau and α-synuclein concentrations were changed significantly in AD, and the ratio of total tau/α-synuclein (N/αS) was dramatically increased in AD than HC. Remarkably, N/αS revealed a strong positive correlation with tau phosphorylation rate. Also, the combination of N/αS with amyloid-β1-42/phosphorylated tau181ratio had the best diagnosis performance (AUC = 0.956, sensitivity = 96%, specificity = 87%). In concordance analysis, N/αS showed the higher diagnostic agreement with amyloid-β1-42 and amyloid-PET. Analysis of biomarker profiling with N/αS had distinctive characteristics and clustering of each group. Especially, among the group of suspected non-Alzheimers disease pathophysiology, all A−T+N+ patients with N/αS+ were reintegrated into AD. Conclusions The high correlation of α-synuclein with tau and the elevated N/αS in AD supported the involvement of α-synuclein in AD pathophysiology. Importantly, N/αS improved the diagnostic performance, confirming the needs of incorporating α-synuclein as a biomarker for neurodegenerative disorders. The incorporation of a biomarker group [N/αS] could contribute to provide better understanding and diagnosis of neurodegenerative disorders