M. Kelley

Manipulating Liquid Metal Droplets in Microfluidic Channels With Minimized Skin Residues Toward Tunable RF Applications

A nontoxic liquid metal, such as eutectic gallium-indium (EGaIn) alloy, has been used to develop tunable radio frequency (RF) components, such as antennas, inductors, or capacitors, for enabling large tunable range, better linearity, and low loss, using fluidic displacement of the liquid metal. However, EGaIn residue, due to its fast oxidation, limits multiple movement of the EGaIn in the reconfigurable RF components. This paper focuses on the use of surfactants, carrier liquids, and microchannel coating materials that minimize EGaIn fragmentation and EGaIn residues on poly(dimethylsiloxane) (PDMS)-based microfluidic channels during repeated actuation of an EGaIn plug. Using a combination of carrier liquids and microchannel coating materials to minimize EGaIn from leaving residues on the PDMS microfluidic channel, a microstrip transmission line switch as a proof-of-concept reconfigurable RF application using the EGaIn plug is demonstrated. It is switched ON<;4 dB and OFF with a loss of <;18 dB over the frequency range between 4 and 15 GHz.

Effects of cytochrome P-450 monooxygenase inducers on mouse hepatic microsomal metabolism of testosterone and alkoxyresorufins

The effects of treatment with phenobarbital, 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP), pregnenolone-16 alpha-carbonitrile (PCN), 3-methylcholanthrene (3-MC) and isosafrole on the hepatic microsomal formation of nine monohydroxy metabolites of testosterone and the O-dealkylation of the ethyl and pentyl ethers of resourfin were evaluated in adult male C57BL/6J and DBA/2NCR mice. In both strains, phenobarbital, TCPOBOP and PCN induced testosterone 2 beta-, 6 beta-, 15 beta- and 16 beta-hydroxylases up to 5-fold, while phenobarbital and TCPOBOP increased the rate of dealkylation of pentoxyresorufin by approximately 30-fold. However, phenobarbital and TCPOBOP did not exhibit identical patterns of induction for the testosterone oxidation reactions. Hepatic microsomes from C57BL/6J mice treated with TCPOBOP displayed a depression in 6 alpha-testosterone hydroxylase activity, which was also observed in PCN-treated animals, whereas phenobarbital-treated mice exhibited an elevation in this monooxygenase activity. A dose of TCPOBOP (0.5 mumol/kg) previously demonstrated to represent an ED50 for mouse aminopyrine N-demethylase activity was also found to approximate the ED50 for pentoxyresorufin O-dealkylase activity in the C57BL/6J mouse. Isosafrole or 3-MC treatment had little effect on testosterone metabolism or pentoxyresorufin O-dealkylase activity in either strain, while 3-MC induced ethoxyresorufin O-deethylase activity in C57BL/6J but not DBA/2NCR mice. This study confirms that TCPOBOP is a potent cytochrome P-450 inducer which most closely resembles phenobarbital in its mode of action. However, TCPOBOP and phenobarbital do not evoke identical modulations of cytochrome P-450-dependent monooxygenases in mice.

1,4-Bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) and related compounds as inducers of hepatic monooxygenases: Structure-activity effects

1,4-Bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) resembles phenobarbital (PB) in its mode of induction of the hepatic drug-metabolizing enzymes in mice. The structural features of this molecule include: a linear tricyclic aromatic ether ring system, an internal 1,4-disubstituted benzene ring and two 3,5-dichloropyridyloxy substituents. Ten analogs of TCPOBOP have been synthesized and their activities as microsomal enzyme inducers evaluated. Dose-response induction of mice hepatic microsomal cytochrome P-450, aldrin epoxidase and dimethylaminoantipyrine N-demethylase gave ED50 values for TCPOBOP and five homologs. The results illustrate that changes in the structure of the pyridyloxy ring markedly affect enzyme induction activity. The order of activity for the substituents was 3,5-dibromopyridyloxy approximately 3,5-dichloropyridyloxy greater than 5-bromopyridyloxy approximately 5-chloropyridyloxy greater than 3-chloropyridyloxy greater than pyridyloxy. In addition, the effects of altered substitution pattern of the benzene ring and structural alterations of the internal ring moiety were evaluated by measuring hepatic microsomal coumarin hydroxylase activity. The results confirm the microsomal monooxygenase enzyme induction activity of TCPOBOP, and the observed structure-dependent potencies of several related homologs support a receptor-mediated mechanism of action for the process.

Liver DNA alterations by 2,3,7,8-tetrachlorodibenzo-p-dioxin and 1,2,3,7,8-pentachlorodibenzo-p-dioxin in the female rat

Abstract 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and 1,2,3,7,8-pentachlorodibenzo-p-dioxin (PCDD) were administered by oral gavage [1 ug/kg/week in corn oil (5 ml/kg)] to female Sprague-Dawley rats for up to six months. Liver and kidney DNA were isolated and the formation of DNA adducts in liver and kidney were determined by the highly sensitive 32p-postlabeling assay procedure. No exposure-related spots associated with TCDD or PCDD covalent DNA adducts were noted on the chromatograms of kidney or liver DNA nucleotides from the rats exposed to the toxins for 2 and 6 months. Corn oil treated animals exhibited the characteristic tissue- and age-specific patterns of 32p-labeled I-spots (Randerath, Reddy and Disher, Carcinogenesis 7, 1615, 1986) which are associated with specific DNA modifications of unknown function. Treatment with either PCDD or TCDD resulted in significant and substantial reduction of the levels of the I-compounds in the liver but not the kidney DNA. Reductions in the amounts of individual hepatic I-compounds ranged from 45–65 and 40–80% in rats treated with TCDD for 2 and 6 months respectively. The effects of PCDD were less marked than those observed for TCDD.

The effects of cytosolic receptor modulation on the AHH-inducing activity of 2,3,7,8-TCDD

Abstract Pretreatment of immature male Wistar rats or C57BL/6J inbred mice for 7 days with 2,2′,4,4′,5,5′-hexachlorobiphenyl (300–500 umol/kg) resulted in a 100 to 300% increase in hepatic levels of the cytosolic receptor protein. This PCB congener exhibits minimal binding affinity for the receptor and does not induce hepatic microsomal aryl hydrocarbon hydroxylase (AHH) or ethoxyresorufin 0-deethylase (EROD). The hepatic microsomal AHH and EROD activities of rats treated with 2,3,7,8-TCDD (0.1 ug/kg) were 240 and 140 pmol product formed/mg protein/min. In contrast, if the rats are pretreated with 2,2′,4,4′,5,5′-hexachlorobiphenyl 7 days prior to intraperitoneal injection of 2,3,7,8-TCDD (0.1 ug/kg) the hepatic AHH and EROD activities were 1400 and 2340 pmol product formed/mg protein/min. Comparable interactive effects of 2,2′,4,4′,5,5′-hexachlorobiphenyl and 2,3,7,8-TCDD were also observed in C57BL/6J mice; hepatic microsomal AHH and EROD activities of mice treated with 2,3,7,8-TCDD (0.32 ug/kg) were 340 and 437 pmol product formed/mg protein/min however these activities were increased to 587 and 1383 pmol product/mg protein/min in mice treated with both 2,3,7,8-TCDD (0.32 ug/kg) and 2,2′,4,4′,5,5t-hexachlorobiphenyl (500 umol/kg). These synergistic effects were observed in rats and mice only at dose levels of 2,3,7,8-TCDD which elicited submaximal AHH and EROD induction responses.

The effects of recptor modulators on the AHH induction activity of 2,3,7,8-TCDD in C57BL/6 and DBA/2 mice

Abstract Treatment of immature male C57BL/6J mice with 2,2′,4,4′,5,5′-hexachlorobiphenyl (HCB, 100–1000 umol/kg) resulted in a 44–200% increase in levels of the 2,3,7,8-TCDD hepatic cytosolic receptor protein for up to 14 days. The increased binding was not due to an alteration of the affinity of 2,3,7,8-TCDD for the receptor as shown by Scatchard analysis. In contrast treatment of immature DBA/2 mice with 2,2′,4,4′,5,5′-HCB did not result in increased hepatic cytosolic receptor levels which were non-detectable in the treated and untreated animals. C57BL/6 mice were pretreated with 2,2′,4,4′,5,5′-HCB (500 umol/kg) and after 7 days 2,3,7,8-TCDD (0.32 ug/kg) was administered by i.p. injection; 14 days later the hepatic microsomal aryl hydrocarbon hydroxylase (AHH) and ethoxyresorufin O-deethylase (EROD) activities were 587 and 1383 pmol product/mg protein/min respectively. In contrast, these activities were 340 and 437 pmol/mg protein/min in animals treated with only 2,3,7,8-TCDD. These synergistic effects were only seen in mice treated with submaximal enzymeinducing doses of 2,3,7,8-TCDD. Treatment of DBA/2 mice with 2,2′,4,4′,5,5′-HCB (500 umol/kg) and varying dose levels of 2,3,7,8-TCDD (10–5000 nmol/kg) resulted in apparent synergistic AHH and EROD induction activities in mice treated with submaximal and maximal enzyme inducing doses of 2,3,7,8-TCDD.

Fluidic tuning of a frequency selective surface based on a four-arm Archimedean spiral

This paper investigates the effects of changing the superstrate above a sub-wavelength Archimedean spiral frequency selective surface. The first part of the paper outlines the design procedure taken to create the FSS geometry for both the band-pass and band-stop. The effects of adding a PDMS bonding layer and a fluidic channel layer above the FSS are investigated and the addition of these layers requires a retuning of the spiral topology. The final part of the paper discusses the effects of dynamically tuning the resonant frequency by changing the effective dielectric constant of the fluids in the superstrate.