1,900 research outputs found

    Resonant diaphragm pressure measurement system with ZnO on Si excitation

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    The principle of measuring pressure by means of a resonant diaphragm has been studied. An oscillator consisting of an integrated amplifier with a piezoelectrically driven diaphragm in its feedback loop has been built. The oscillator frequency is accurately proportional to the square of the pressure in the range of 60 to 130 Torr.\ud The frequency range is 1324 to 1336 Hz (this range being limited by a spurious mode which could be suppressed by better processing) for a 25 mm diameter diaphragm made of a silicon wafer and with PZT ceramics as driver and receptor. We have made an integrated version (1 × 1 mm2) of a square resonant diaphragm pressure guage by selective etching of (1 0 0) planes with ethylenediamine. The piezoelectric driving materials was sputtered zinc oxide. A driver was deposited midway between the bending point and the point of greatest curvature.\ud A receptor was located at a symmetrical position to give a optimum transfer condition.\ud The integrated current amplifier had a low impedance differential input stage, two gain cells and a high impedance output stage. These electrical conditions ensured maximum elastic freedom of the diaphragm. A digital circuit in I2L technology has been designed and made with eight-bit parallel read out of the frequency. This circuit may be directly connected to a microprocessor. The whole system contains the sensor chip, the analog amplifier chip and the digital chip, all in compatible technology.\ud \u

    Vaginal Microbicides: Detecting Toxicities in Vivo that Paradoxically Increase Pathogen Transmission

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    BACKGROUND: Microbicides must protect against STD pathogens without causing unacceptable toxic effects. Microbicides based on nonoxynol-9 (N9) and other detergents disrupt sperm, HSV and HIV membranes, and these agents are effective contraceptives. But paradoxically N9 fails to protect women against HIV and other STD pathogens, most likely because it causes toxic effects that increase susceptibility. The mouse HSV-2 vaginal transmission model reported here: (a) Directly tests for toxic effects that increase susceptibility to HSV-2, (b) Determines in vivo whether a microbicide can protect against HSV-2 transmission without causing toxicities that increase susceptibility, and (c) Identifies those toxic effects that best correlate with the increased HSV susceptibility. METHODS: Susceptibility was evaluated in progestin-treated mice by delivering a low-dose viral inoculum (0.1 ID50) at various times after delivering the candidate microbicide to detect whether the candidate increased the fraction of mice infected. Ten agents were tested – five detergents: nonionic (N9), cationic (benzalkonium chloride, BZK), anionic (sodium dodecylsulfate, SDS), the pair of detergents in C31G (C14AO and C16B); one surface active agent (chlorhexidine); two non-detergents (BufferGel®, and sulfonated polystyrene, SPS); and HEC placebo gel (hydroxyethylcellulose). Toxic effects were evaluated by histology, uptake of a 'dead cell' dye, colposcopy, enumeration of vaginal macrophages, and measurement of inflammatory cytokines. RESULTS: A single dose of N9 protected against HSV-2 for a few minutes but then rapidly increased susceptibility, which reached maximum at 12 hours. When applied at the minimal concentration needed for brief partial protection, all five detergents caused a subsequent increase in susceptibility at 12 hours of ~20–30-fold. Surprisingly, colposcopy failed to detect visible sign of the N9 toxic effect that increased susceptibility at 12 hours. Toxic effects that occurred contemporaneously with increased susceptibility were rapid exfoliation and re-growth of epithelial cell layers, entry of macrophages into the vaginal lumen, and release of one or more inflammatory cytokines (Il-1β, KC, MIP 1α, RANTES). The non-detergent microbicides and HEC placebo caused no significant increase in susceptibility or toxic effects. CONCLUSION: This mouse HSV-2 model provides a sensitive method to detect microbicide-induced toxicities that increase susceptibility to infection. In this model, there was no concentration at which detergents provided protection without significantly increasing susceptibility.JHU Woodrow Wilson Fellowship; National Institutes of Health (Program Project A1 45967

    A Single-Trim frequency reference system with 0.7 ppm/°C from −63 °C to 165 °C Consuming 210 μW at 70 MHz

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    This article presents a frequency reference system that combines high frequency accuracy and low power consumption using a single-point temperature trim and batch calibration. The system is intended as a low-cost fully integrated crystal oscillator replacement. In this system, the oscillation frequency of a power-efficient, but process, voltage, temperature (PVT) and lifetime (L)-sensitive current-controlled ring oscillator (CCO) is periodically (re)calibrated by the well-behaved frequency stability of an untuned LC -based Colpitts oscillator (LCO), which is optimized for stability over PVT variations and lifetime (PVTL). During the single-point room temperature factory trim, the frequency of the LCO is determined and the result is digitally stored. An on-chip calibration engine tunes the CCO to the target frequency based on the LCO frequency, temperature sensor information, and digitally stored trimming information, thus effectively improving the frequency stability of the ring oscillator. The relatively high-power LCO is heavily duty-cycled to minimize the overall power consumption. A prototype fabricated in a 0.13- μ m high-voltage (HV) CMOS SOI process and assembled in a plastic package demonstrates an inaccuracy lower than ±93 ppm over a temperature range from -63 °C to 165 °C across 18 samples. The presented frequency reference system, including on-chip voltage regulators and a temperature sensor, occupies a chip area of 0.69 mm2 and consumes about 64 μA from a single 3.3-V supply. The frequency error due to supply variation is roughly 92 ppm/V. The mean frequency shift due to aging, measured before and after a six-day storage bake at 175 °C, is only 52 ppm.</p

    Epidemic Wave Dynamics Attributable to Urban Community Structure: A Theoretical Characterization of Disease Transmission in a Large Network.

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    BACKGROUND: Multiple waves of transmission during infectious disease epidemics represent a major public health challenge, but the ecological and behavioral drivers of epidemic resurgence are poorly understood. In theory, community structure—aggregation into highly intraconnected and loosely interconnected social groups—within human populations may lead to punctuated outbreaks as diseases progress from one community to the next. However, this explanation has been largely overlooked in favor of temporal shifts in environmental conditions and human behavior and because of the difficulties associated with estimating large-scale contact patterns. OBJECTIVE: The aim was to characterize naturally arising patterns of human contact that are capable of producing simulated epidemics with multiple wave structures. METHODS: We used an extensive dataset of proximal physical contacts between users of a public Wi-Fi Internet system to evaluate the epidemiological implications of an empirical urban contact network. We characterized the modularity (community structure) of the network and then estimated epidemic dynamics under a percolation-based model of infectious disease spread on the network. We classified simulated epidemics as multiwave using a novel metric and we identified network structures that were critical to the network's ability to produce multiwave epidemics. RESULTS: We identified robust community structure in a large, empirical urban contact network from which multiwave epidemics may emerge naturally. This pattern was fueled by a special kind of insularity in which locally popular individuals were not the ones forging contacts with more distant social groups. CONCLUSIONS: Our results suggest that ordinary contact patterns can produce multiwave epidemics at the scale of a single urban area without the temporal shifts that are usually assumed to be responsible. Understanding the role of community structure in epidemic dynamics allows officials to anticipate epidemic resurgence without having to forecast future changes in hosts, pathogens, or the environment
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